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Nielsen MB, Benn M, Nordestgaard BG, Skov L, Çolak Y. Adiponectin and Risk of Psoriasis: Observational and Mendelian Randomization Studies in up to 900 000 Individuals. Clin Chem 2025; 71:286-295. [PMID: 39478357 DOI: 10.1093/clinchem/hvae160] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [MESH Headings] [Grants] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 07/06/2024] [Accepted: 09/10/2024] [Indexed: 02/04/2025]
Abstract
BACKGROUND Psoriasis is a chronic inflammatory skin disorder often associated with obesity. Adiponectin, an anti-inflammatory protein-hormone secreted by adipose tissue, may be a link between obesity and psoriasis. We hypothesized that low plasma adiponectin is associated with an increased risk of psoriasis in observational and causal genetic studies. METHODS In observational analyses, we used information on plasma adiponectin and psoriasis in 30 045 individuals from the Copenhagen General Population Study (CGPS). In one-sample Mendelian randomization analyses, we used genetic information on adiponectin and psoriasis in 107 308 individuals from the CGPS. In two-sample Mendelian randomization analyses, we used genetic information on adiponectin from the ADIPOGen consortium and genetic information on psoriasis in 373 338 and 462 933 individuals from the FinnGen study and UK Biobank (UKB). RESULTS In observational analyses, a 1-unit log-transformed higher plasma adiponectin was associated with a hazard ratio (HR) for psoriasis of 0.67 (95% confidence interval: 0.48-0.94) in an age- and sex-adjusted model but not in a multivariable adjusted model including obesity measures with a HR of 0.95 (0.66-1.35). In genetic one-sample Mendelian randomization analysis, a 1-unit log-transformed higher plasma adiponectin was not associated with a causal risk ratio for psoriasis of 1.33 (0.77-2.32) in the CGPS. In two-sample Mendelian randomization analyses, a 1-unit log-transformed higher plasma adiponectin was not associated with causal risk ratios for psoriasis of 0.96 (0.81-1.14) in FinnGen and 1.00 (1.00-1.01) in UKB. CONCLUSIONS Low plasma adiponectin is associated with increased risk of psoriasis in age- and sex-adjusted observational analyses; however, this was not the case after adjustment for obesity measures or in causal genetic analyses.
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Affiliation(s)
- Maria B Nielsen
- Department of Clinical Biochemistry, Copenhagen University Hospital-Herlev and Gentofte, Copenhagen, Denmark
- The Copenhagen General Population Study, Copenhagen University Hospital-Herlev and Gentofte, Copenhagen, Denmark
- Department of Clinical Medicine, Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark
- Department of Dermatology and Allergy, Copenhagen University Hospital-Herlev and Gentofte, Copenhagen, Denmark
| | - Marianne Benn
- The Copenhagen General Population Study, Copenhagen University Hospital-Herlev and Gentofte, Copenhagen, Denmark
- Department of Clinical Medicine, Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark
- Department of Clinical Biochemistry, Copenhagen University Hospital-Rigshospitalet, Copenhagen, Denmark
| | - Børge G Nordestgaard
- Department of Clinical Biochemistry, Copenhagen University Hospital-Herlev and Gentofte, Copenhagen, Denmark
- The Copenhagen General Population Study, Copenhagen University Hospital-Herlev and Gentofte, Copenhagen, Denmark
- Department of Clinical Medicine, Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark
| | - Lone Skov
- Department of Clinical Medicine, Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark
- Department of Dermatology and Allergy, Copenhagen University Hospital-Herlev and Gentofte, Copenhagen, Denmark
| | - Yunus Çolak
- The Copenhagen General Population Study, Copenhagen University Hospital-Herlev and Gentofte, Copenhagen, Denmark
- Department of Clinical Medicine, Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark
- Department of Respiratory Medicine, Copenhagen University Hospital-Herlev and Gentofte, Copenhagen, Denmark
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Duan F, Wu J, Chang J, Peng H, Liu Z, Liu P, Han X, Sun T, Shang D, Yang Y, Li Z, Li P, Liu Y, Zhu Y, Lv Y, Guo X, Zhao Y, An Y. Deciphering endocrine function of adipose tissue and its significant influences in obesity-related diseases caused by its dysfunction. Differentiation 2025; 141:100832. [PMID: 39709882 DOI: 10.1016/j.diff.2024.100832] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 10/29/2024] [Revised: 12/15/2024] [Accepted: 12/16/2024] [Indexed: 12/24/2024]
Abstract
Current research has found that adipose tissue is not only involved in energy metabolism, but also a highly active endocrine organ that secretes various adipokines, including adiponectin, leptin, resistin and apelin, which are involved in the regulation of physiology and pathology of tissues and organs throughout the body. With the yearly increasing incidence, obesity has become a risk factor for a variety of pathological changes, including inflammation and metabolic syndrome in various system (endocrine, circulatory, locomotor and central nervous system). Thus these symptoms lead to multi-organ dysfunctions, including the heart, liver, kidneys, brain and joints. An in-depth summary of the roles of adipokines in the regulation of other tissues and organs can help to provide more effective therapeutic strategies for obesity-related diseases and explore potential therapeutic targets. Therefore, this review has retrospected the endocrine function of adipose tissue under obesity and the role of dysregulated adipokine secretion in related diseases and the underlying mechanisms, in order to provide a theoretical basis for targeting adipokine-mediated systemic dysregulation.
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Affiliation(s)
- Feiyi Duan
- Department of Biochemistry and Molecular Biology, School of Basic Medical Sciences, Henan University, Kaifeng, 475004, China; Henan Provincial Engineering Center for Tumor Molecular Medicine, Kaifeng Key Laboratory of Cell Signal Transduction, Henan University, Kaifeng, 475004, China
| | - Jiaoyan Wu
- Department of Biochemistry and Molecular Biology, School of Basic Medical Sciences, Henan University, Kaifeng, 475004, China; Henan Provincial Engineering Center for Tumor Molecular Medicine, Kaifeng Key Laboratory of Cell Signal Transduction, Henan University, Kaifeng, 475004, China
| | - Jiayi Chang
- Department of Biochemistry and Molecular Biology, School of Basic Medical Sciences, Henan University, Kaifeng, 475004, China; Henan Provincial Engineering Center for Tumor Molecular Medicine, Kaifeng Key Laboratory of Cell Signal Transduction, Henan University, Kaifeng, 475004, China
| | - Haoyuan Peng
- Department of Biochemistry and Molecular Biology, School of Basic Medical Sciences, Henan University, Kaifeng, 475004, China; Henan Provincial Engineering Center for Tumor Molecular Medicine, Kaifeng Key Laboratory of Cell Signal Transduction, Henan University, Kaifeng, 475004, China
| | - Zitao Liu
- Department of Biochemistry and Molecular Biology, School of Basic Medical Sciences, Henan University, Kaifeng, 475004, China; Henan Provincial Engineering Center for Tumor Molecular Medicine, Kaifeng Key Laboratory of Cell Signal Transduction, Henan University, Kaifeng, 475004, China
| | - Pengfei Liu
- Department of Biochemistry and Molecular Biology, School of Basic Medical Sciences, Henan University, Kaifeng, 475004, China; Henan Provincial Engineering Center for Tumor Molecular Medicine, Kaifeng Key Laboratory of Cell Signal Transduction, Henan University, Kaifeng, 475004, China
| | - Xu Han
- Department of Biochemistry and Molecular Biology, School of Basic Medical Sciences, Henan University, Kaifeng, 475004, China; School of Stomatology, Henan University, Kaifeng, 475004, China
| | - Tiantian Sun
- Department of Biochemistry and Molecular Biology, School of Basic Medical Sciences, Henan University, Kaifeng, 475004, China; School of Stomatology, Henan University, Kaifeng, 475004, China
| | - Dandan Shang
- Department of Biochemistry and Molecular Biology, School of Basic Medical Sciences, Henan University, Kaifeng, 475004, China; Henan Provincial Engineering Center for Tumor Molecular Medicine, Kaifeng Key Laboratory of Cell Signal Transduction, Henan University, Kaifeng, 475004, China
| | - Yutian Yang
- Department of Biochemistry and Molecular Biology, School of Basic Medical Sciences, Henan University, Kaifeng, 475004, China; Henan Provincial Engineering Center for Tumor Molecular Medicine, Kaifeng Key Laboratory of Cell Signal Transduction, Henan University, Kaifeng, 475004, China
| | - Zhihao Li
- Department of Biochemistry and Molecular Biology, School of Basic Medical Sciences, Henan University, Kaifeng, 475004, China; Henan Provincial Engineering Center for Tumor Molecular Medicine, Kaifeng Key Laboratory of Cell Signal Transduction, Henan University, Kaifeng, 475004, China
| | - Pengkun Li
- Department of Biochemistry and Molecular Biology, School of Basic Medical Sciences, Henan University, Kaifeng, 475004, China; Henan Provincial Engineering Center for Tumor Molecular Medicine, Kaifeng Key Laboratory of Cell Signal Transduction, Henan University, Kaifeng, 475004, China
| | - Yixuan Liu
- Department of Biochemistry and Molecular Biology, School of Basic Medical Sciences, Henan University, Kaifeng, 475004, China; Henan Provincial Engineering Center for Tumor Molecular Medicine, Kaifeng Key Laboratory of Cell Signal Transduction, Henan University, Kaifeng, 475004, China
| | - Yonghao Zhu
- Department of Biochemistry and Molecular Biology, School of Basic Medical Sciences, Henan University, Kaifeng, 475004, China; School of Stomatology, Henan University, Kaifeng, 475004, China
| | - Yunzhi Lv
- Department of Biochemistry and Molecular Biology, School of Basic Medical Sciences, Henan University, Kaifeng, 475004, China; School of Stomatology, Henan University, Kaifeng, 475004, China
| | - Xiumei Guo
- Department of Biochemistry and Molecular Biology, School of Basic Medical Sciences, Henan University, Kaifeng, 475004, China; Henan Provincial Engineering Center for Tumor Molecular Medicine, Kaifeng Key Laboratory of Cell Signal Transduction, Henan University, Kaifeng, 475004, China
| | - Ying Zhao
- Department of Biochemistry and Molecular Biology, School of Basic Medical Sciences, Henan University, Kaifeng, 475004, China; Henan Provincial Engineering Center for Tumor Molecular Medicine, Kaifeng Key Laboratory of Cell Signal Transduction, Henan University, Kaifeng, 475004, China
| | - Yang An
- Department of Biochemistry and Molecular Biology, School of Basic Medical Sciences, Henan University, Kaifeng, 475004, China; Henan Provincial Engineering Center for Tumor Molecular Medicine, Kaifeng Key Laboratory of Cell Signal Transduction, Henan University, Kaifeng, 475004, China.
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Myasoedova VA, Bertolini F, Valerio V, Moschetta D, Massaiu I, Rusconi V, De Giorgi D, Ciccarelli M, Parisi V, Poggio P. The Role of Adiponectin and Leptin in Fibro-Calcific Aortic Valve Disease: A Systematic Review and Meta-Analysis. Biomedicines 2024; 12:1977. [PMID: 39335491 PMCID: PMC11428218 DOI: 10.3390/biomedicines12091977] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [Grants] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 07/10/2024] [Revised: 08/12/2024] [Accepted: 08/13/2024] [Indexed: 09/30/2024] Open
Abstract
BACKGROUND Fibro-calcific aortic valve disease (FCAVD) is a progressive disorder characterized by the thickening and calcification of the aortic valve, eventually leading to aortic stenosis. Adiponectin and leptin, known for their anti-inflammatory and proinflammatory properties, respectively, have been implicated in cardiovascular diseases, but their associations with FCAVD are controversial. This meta-analysis aims to evaluate the relationships between adiponectin and leptin levels and FCAVD, particularly in patients with severe aortic stenosis (AS). METHODS A systematic search was conducted across the PubMed, Scopus, and Web of Science databases to identify studies on adiponectin and leptin levels in FCAVD. The methodological quality of each study was assessed using the Newcastle-Ottawa Scale. Standardized mean differences (SMDs) and 95% confidence intervals (CIs) were calculated, and publication bias was evaluated using Egger's test and funnel plots. RESULTS Out of 191 articles identified, 10 studies involving 2360 patients (989 with FCAVD and 1371 controls) were included. The analysis suggested trends in the associations of lower adiponectin levels (SMD = -0.143, 95% CI: -0.344, 0.057, p = 0.161) and higher leptin levels (SMD = 0.175, 95% CI: -0.045, 0.395, p = 0.119) with FCAVD. The association remained a trend for low adiponectin but showed a significant correlation with high leptin in severe AS patients (SMD = 0.29, 95% CI: 0.036, 0.543, p = 0.025). CONCLUSION This meta-analysis indicates a potential association between elevated leptin levels and severe aortic stenosis, while the relationship with adiponectin levels remains inconclusive. These findings highlight the need for further and dedicated research to clarify the roles of these adipokines in the pathogenesis of FCAVD and their potential roles as biomarkers for disease progression.
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Affiliation(s)
| | | | | | | | | | | | | | - Michele Ciccarelli
- Department of Medicine, Surgery and Dentistry, University of Salerno, 84084 Fisciano, Italy
| | - Valentina Parisi
- Department of Translational Medical Sciences, Federico II University, 80138 Naples, Italy
| | - Paolo Poggio
- Centro Cardiologico Monzino IRCCS, 20138 Milan, Italy
- Department of Biomedical, Surgical and Dental Sciences, University of Milan, 20122 Milan, Italy
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Klobučar I, Habisch H, Klobučar L, Trbušić M, Pregartner G, Berghold A, Kostner GM, Scharnagl H, Madl T, Frank S, Degoricija V. Sex-Related Differences in the Associations between Adiponectin and Serum Lipoproteins in Healthy Subjects and Patients with Metabolic Syndrome. Biomedicines 2024; 12:1972. [PMID: 39335486 PMCID: PMC11429094 DOI: 10.3390/biomedicines12091972] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [Grants] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 07/26/2024] [Revised: 08/23/2024] [Accepted: 08/28/2024] [Indexed: 09/30/2024] Open
Abstract
The strong associations between the serum levels of adiponectin and the lipoprotein subclasses observed in healthy subjects are much weaker in patients with metabolic syndrome (MS). However, the impact of sex on these associations remained unexplored. Therefore, in the present study, we examined associations between adiponectin and the lipoprotein subclasses, analyzed by nuclear magnetic resonance spectroscopy, separately in healthy females and males, as well as in females and males with MS. We observed negative correlations between adiponectin and VLDL, IDL, and small-dense LDL in healthy males, but neither in healthy females nor in females or males with MS. Additionally, adiponectin was positively correlated with some HDL subclasses in healthy males and females with MS, but not in healthy females or males with MS. Adjusting for age and either body mass index, waist circumference, C-reactive protein, or interleukin-6 weakened the associations between adiponectin and VLDL and IDL but not small-dense LDL. The adjustment weakened the associations between adiponectin and HDL in healthy males but not in females with MS. Based on our results, we conclude that sex and the presence of MS are strong determinants of the associations between adiponectin and serum lipoproteins and that the complex regulatory network comprising adiponectin and other molecular players involved in the regulation of lipoprotein metabolism is primarily operative in healthy males and females with MS.
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Affiliation(s)
- Iva Klobučar
- Department of Cardiology, Sisters of Charity University Hospital Centre, 10000 Zagreb, Croatia; (I.K.); (M.T.)
| | - Hansjörg Habisch
- Otto Loewi Research Center, Medicinal Chemistry, Medical University of Graz, 8010 Graz, Austria; (H.H.); (T.M.)
| | - Lucija Klobučar
- Department of Medicine, University Hospital Centre Osijek, 31000 Osijek, Croatia;
| | - Matias Trbušić
- Department of Cardiology, Sisters of Charity University Hospital Centre, 10000 Zagreb, Croatia; (I.K.); (M.T.)
- School of Medicine, University of Zagreb, 10000 Zagreb, Croatia;
| | - Gudrun Pregartner
- Institute for Medical Informatics, Statistics, and Documentation, Medical University of Graz, 8036 Graz, Austria; (G.P.); (A.B.)
| | - Andrea Berghold
- Institute for Medical Informatics, Statistics, and Documentation, Medical University of Graz, 8036 Graz, Austria; (G.P.); (A.B.)
| | - Gerhard M. Kostner
- Gottfried Schatz Research Center, Molecular Biology and Biochemistry, Medical University of Graz, 8010 Graz, Austria;
| | - Hubert Scharnagl
- Clinical Institute of Medical and Chemical Laboratory Diagnostics, Medical University of Graz, 8036 Graz, Austria;
| | - Tobias Madl
- Otto Loewi Research Center, Medicinal Chemistry, Medical University of Graz, 8010 Graz, Austria; (H.H.); (T.M.)
- BioTechMed-Graz, 8010 Graz, Austria
| | - Saša Frank
- Gottfried Schatz Research Center, Molecular Biology and Biochemistry, Medical University of Graz, 8010 Graz, Austria;
- BioTechMed-Graz, 8010 Graz, Austria
| | - Vesna Degoricija
- School of Medicine, University of Zagreb, 10000 Zagreb, Croatia;
- Department of Medicine, Sisters of Charity University Hospital Centre, 10000 Zagreb, Croatia
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Alenezi SA, Elkmeshi N, Alanazi A, Alanazi ST, Khan R, Amer S. The Impact of Diet-Induced Weight Loss on Inflammatory Status and Hyperandrogenism in Women with Polycystic Ovarian Syndrome (PCOS)-A Systematic Review and Meta-Analysis. J Clin Med 2024; 13:4934. [PMID: 39201076 PMCID: PMC11355208 DOI: 10.3390/jcm13164934] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 07/24/2024] [Revised: 08/12/2024] [Accepted: 08/16/2024] [Indexed: 09/02/2024] Open
Abstract
Background: Currently, the primary strategy for addressing polycystic ovarian syndrome (PCOS) involves lifestyle modifications, with a focus on weight loss. The purpose of this meta-analysis was to assess the impact of weight loss through dietary interventions on inflammatory status and hyperandrogenism in PCOS women. Methods: A comprehensive search was conducted to identify randomised controlled trials (RCTs) and cohort studies assessing the impact of diet-induced weight loss on circulating inflammatory markers (CRP, IL-6, IL-1β, TNF-α), androgens (testosterone, androstenedione), SHBG, and luteinising hormone (LH) in PCOS women. The quality and risk of bias of the included studies were assessed using the Cochrane Collaboration's tool for RCTs and the Newcastle-Ottawa Scale for cohort studies. Data were entered into RevMan software v5.9 for the calculation of standard mean difference (SMD) and the 95% confidence interval (95%CI) of circulating inflammatory markers, androgens, and LH between baseline and post-weight loss values. Results: Eleven studies (n = 323) were eligible for the systematic review, of which nine (n = 286) were included in the meta-analysis. Pooled analysis of data revealed a statistically significant decrease in circulating CRP (SMD 0.39, 95%CI 0.22, 0.56; 9 studies, n = 286), IL-6 (SMD 0.37, 95%Cl, 0.12, 0.61; 3 Studies, n = 140), TNF-α (SMD 0.30, 95%Cl, 0.07, 0.53; 4 Studies, n = 162), androstenedione (SMD 0.36, 95%Cl, 0.13, 0.60; 4 studies, n = 147) and LH (SMD 0.30, 95% Cl, 0.09, 0.51; 5 studies, n = 197) after weight loss compared to baseline levels among PCOS women. A meta-analysis of five studies (n = 173) showed a statistically significant increase in circulating SHBG after weight loss compared to baseline levels (SMD -0.43, 95%Cl, -0.65, -0.21). Conclusions: These findings suggest that weight loss induced by dietary interventions seems to improve PCOS-related chronic inflammation and hyperandrogenism. The possible causative relationship between the improvement in inflammation and hyperandrogenism remains to be determined.
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Affiliation(s)
- Salih Atalah Alenezi
- Division of Translational Medical Sciences, School of Medicine, University of Nottingham, Nottingham NG5 1PB, UK or (S.A.A.); (N.E.); (R.K.)
- Prince Mohammed Bin Abdulaziz Medical City, Ministry of Health, Riyadh 14214, Saudi Arabia
| | - Nusaiba Elkmeshi
- Division of Translational Medical Sciences, School of Medicine, University of Nottingham, Nottingham NG5 1PB, UK or (S.A.A.); (N.E.); (R.K.)
| | - Abdullah Alanazi
- Health Sciences, Applied Sciences, Petaling Jaya 47301, Malaysia; (A.A.); (S.T.A.)
| | - Sulaiman T. Alanazi
- Health Sciences, Applied Sciences, Petaling Jaya 47301, Malaysia; (A.A.); (S.T.A.)
| | - Raheela Khan
- Division of Translational Medical Sciences, School of Medicine, University of Nottingham, Nottingham NG5 1PB, UK or (S.A.A.); (N.E.); (R.K.)
| | - Saad Amer
- Division of Translational Medical Sciences, School of Medicine, University of Nottingham, Nottingham NG5 1PB, UK or (S.A.A.); (N.E.); (R.K.)
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Xiang X, Wang D, Leng J, Li N, Wei C. Association of adiponectin and its receptor gene polymorphisms with the risk of coronary heart disease in northern Guangxi. Cytokine 2024; 178:156567. [PMID: 38489870 DOI: 10.1016/j.cyto.2024.156567] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 11/21/2022] [Revised: 02/06/2024] [Accepted: 03/01/2024] [Indexed: 03/17/2024]
Abstract
OBJECTIVE To investigate the association of circulating adiponectin (APN) level and single nucleotide polymorphisms (rs1501299 and rs266729) of the APN gene in the coronary heart disease (CHD) population of Northern Guangxi Province. METHODS Two hundred and sixty-three CHD patients and 235 healthy controls from our hospital from August 2018 to October 2020 were included in this study. ELISA was used to determine the serum APN concentration. PCR-RFLP and direct DNA sequencing were used to analyze the genotypes of APN gene rs1501299 G/T and rs266729 C/G single-nucleotide loci, their distribution differences between the two groups were compared and their correlation with APN concentration was analyzed. RESULTS The serum APN concentration in the CHD group was significantly lower than the control group (14.40(1.42-52.26) μg/mL vs. 29.40 (3.18-90.31) μg/mL, P < 0.001). There were statistically significant differences in the rs266729 genotype of APN single nucleotide locus between the two groups (P < 0.001). The dominant model and recessive model of rs266729 genotype showed that mutant homozygous GG genotype carriers significantly increased the risk of CHD in comparison with C allele carriers (CG + CC) (OR = 2.156, 95 %CI: 1.004-4.631, P = 0.049), and this effect was still significant after adjusting gender and age (OR = 2.695, 95 %CI 1.110-6.540, P = 0.028). In both the dominant and recessive models for rs1501299, ORs before and after adjustment for age and sex revealed no significant association with CHD, with ORs of 0.765 (95 % CI: 0.537-1.091, P = 0.139) and 0.718 (95 % CI: 0.466-1.106, P = 0.133) in the Dominant model, and ORs of 0.960 (95 % CI: 0.442-2.087, P = 0.918) and 0.613 (95 % CI: 0.239-1.570, P = 0.308) in the Recessive model, respectively. No statistically significant differences in APN concentrations across genotypes in both groups (P > 0.05), with chi-square values of 1.633 (control group) and 0.823 (CHD group) for rs1501299, and 1.354 (control group) and 0.618 (CHD group) for rs266729. CONCLUSIONS APN gene of rs266729 C/G single-nucleotide loci gene mutation can significantly increase the risk of CHD. There was no significant correlation between rs1501299 G/T single-nucleotide loci and CHD in Northern Guangxi populations.
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Affiliation(s)
- Xiaohua Xiang
- Department of Laboratory Medicine, Shenzhen Guangming District People's Hospital, Shenzhen 518106, Guangdong Province, China; Department of Laboratory Medicine, The Second Affiliated Hospital of Guilin Medical University, Guilin 541199, Guangxi Province, China.
| | - Di Wang
- Department of Laboratory Medicine, The Second Affiliated Hospital of Guilin Medical University, Guilin 541199, Guangxi Province, China
| | - Jun Leng
- Department of Laboratory Medicine, The Second Affiliated Hospital of Guilin Medical University, Guilin 541199, Guangxi Province, China
| | - Ning Li
- Department of Laboratory Medicine, The Second Affiliated Hospital of Guilin Medical University, Guilin 541199, Guangxi Province, China
| | - Chuandong Wei
- Department of Laboratory Medicine, The Second Affiliated Hospital of Guilin Medical University, Guilin 541199, Guangxi Province, China.
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Zhao YQ, Ren YF, Li BB, Wei C, Yu B. The mysterious association between adiponectin and endometriosis. Front Pharmacol 2024; 15:1396616. [PMID: 38813109 PMCID: PMC11133721 DOI: 10.3389/fphar.2024.1396616] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 03/06/2024] [Accepted: 04/29/2024] [Indexed: 05/31/2024] Open
Abstract
Adiponectin is a pleiotropic cytokine predominantly derived from adipose tissue. In addition to its role in regulating energy metabolism, adiponectin may also be related to estrogen-dependent diseases, and many studies have confirmed its involvement in mediating diverse biological processes, including apoptosis, autophagy, inflammation, angiogenesis, and fibrosis, all of which are related to the pathogenesis of endometriosis. Although many researchers have reported low levels of adiponectin in patients with endometriosis and suggested that it may serve as a protective factor against the development of the disease. Therefore, the purpose of this review was to provide an up-to-date summary of the roles of adiponectin and its downstream cytokines and signaling pathways in the aforementioned biological processes. Further systematic studies on the molecular and cellular mechanisms of action of adiponectin may provide novel insights into the pathophysiology of endometriosis as well as potential therapeutic targets.
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Affiliation(s)
| | | | - Bing-Bing Li
- College of Integrated Chinese and Western Medicine, Jining Medical University, Jining, Shandong Province, China
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Zhu X, Ma E, Ge Y, Yuan M, Guo X, Peng J, Zhu W, Ren DN, Wo D. Resveratrol protects against myocardial ischemic injury in obese mice via activating SIRT3/FOXO3a signaling pathway and restoring redox homeostasis. Biomed Pharmacother 2024; 174:116476. [PMID: 38520872 DOI: 10.1016/j.biopha.2024.116476] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 12/12/2023] [Revised: 03/08/2024] [Accepted: 03/19/2024] [Indexed: 03/25/2024] Open
Abstract
BACKGROUND Increasing global overweight and obesity rates not only increase the prevalence of myocardial infarction (MI), but also exacerbate ischemic injury and result in worsened prognosis. Currently, there are no drugs that can reverse myocardial damage once MI has occurred, therefore discovering drugs that can potentially limit the extent of ischemic damage to the myocardium is critical. Resveratrol is a polyphenol known for its antioxidant properties, however whether prolonged daily intake of resveratrol during obesity can protect against MI-induced damage remains unexplored. METHODS We established murine models of obesity via high-fat/high-fructose diet, along with daily administrations of resveratrol or vehicle, then performed surgical MI to examine the effects and mechanisms of resveratrol in protecting against myocardial ischemic injury. RESULTS Daily administration of resveratrol in obese mice robustly protected against myocardial ischemic injury and improved post-MI cardiac function. Resveratrol strongly inhibited oxidative and DNA damage via activating SIRT3/FOXO3a-dependent antioxidant enzymes following MI, which were completely prevented upon administration of 3-TYP, a selective SIRT3 inhibitor. Hence, the cardioprotective effects of prolonged resveratrol intake in protecting obese mice against myocardial ischemic injury was due to reestablishment of intracellular redox homeostasis through activation of SIRT3/FOXO3a signaling pathway. CONCLUSION Our findings provide important new evidence that supports the daily intake of resveratrol, especially in those overweight or obese, which can robustly decrease the extent of ischemic damage following MI. Our study therefore provides new mechanistic insight and suggests the therapeutic potential of resveratrol as an invaluable drug in the treatment of ischemic heart diseases.
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Affiliation(s)
- Xi Zhu
- Fujian Key Laboratory of Integrative Medicine on Geriatric, Academy of Integrative Medicine, Fujian University of Traditional Chinese Medicine, Fuzhou, Fujian, China
| | - En Ma
- Fujian Key Laboratory of Integrative Medicine on Geriatric, Academy of Integrative Medicine, Fujian University of Traditional Chinese Medicine, Fuzhou, Fujian, China
| | - Yixuan Ge
- Fujian Key Laboratory of Integrative Medicine on Geriatric, Academy of Integrative Medicine, Fujian University of Traditional Chinese Medicine, Fuzhou, Fujian, China
| | - Meng Yuan
- Fujian Key Laboratory of Integrative Medicine on Geriatric, Academy of Integrative Medicine, Fujian University of Traditional Chinese Medicine, Fuzhou, Fujian, China
| | - Xiaowei Guo
- Fujian Key Laboratory of Integrative Medicine on Geriatric, Academy of Integrative Medicine, Fujian University of Traditional Chinese Medicine, Fuzhou, Fujian, China
| | - Jun Peng
- Fujian Key Laboratory of Integrative Medicine on Geriatric, Academy of Integrative Medicine, Fujian University of Traditional Chinese Medicine, Fuzhou, Fujian, China
| | - Weidong Zhu
- Fujian Key Laboratory of Integrative Medicine on Geriatric, Academy of Integrative Medicine, Fujian University of Traditional Chinese Medicine, Fuzhou, Fujian, China; Innovation and Transformation Center, Fujian University of Traditional Chinese Medicine, Fuzhou, Fujian, China
| | - Dan-Ni Ren
- Fujian Key Laboratory of Integrative Medicine on Geriatric, Academy of Integrative Medicine, Fujian University of Traditional Chinese Medicine, Fuzhou, Fujian, China.
| | - Da Wo
- Fujian Key Laboratory of Integrative Medicine on Geriatric, Academy of Integrative Medicine, Fujian University of Traditional Chinese Medicine, Fuzhou, Fujian, China; Innovation and Transformation Center, Fujian University of Traditional Chinese Medicine, Fuzhou, Fujian, China.
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Hashimoto T, Hirano K. Effects of mifepristone on adipocyte differentiation in mouse 3T3-L1 cells. Cell Mol Biol Lett 2024; 29:45. [PMID: 38553665 PMCID: PMC10981365 DOI: 10.1186/s11658-024-00559-9] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Grants] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 12/27/2023] [Accepted: 02/29/2024] [Indexed: 04/01/2024] Open
Abstract
BACKGROUND Both glucocorticoid receptor and peroxisome proliferator-activated receptor-γ (PPARγ) play a critical role in adipocyte differentiation. Mifepristone is not only an antagonist of the glucocorticoid receptor but also an agonist of PPARγ. Therefore, the present study investigated the effect of mifepristone on adipocyte differentiation. METHODS Mouse 3T3-L1 cells were used as a model for adipocyte differentiation. The lipid droplet formation was evaluated with Bodipy493/503 staining and the expression of adipocyte markers [adiponectin and adipocyte fatty acid binding protein-4 (Fabp4)] was evaluated with quantitative PCR and immunoblot analyses for indication of adipocyte differentiation. siRNA and neutralizing antibodies were used to elucidate the molecular mechanism of mifepristone-induced adipocyte differentiation. Luciferase reporter assay was used to examine the effect of mifepristone on the promoter activity of PPAR-response element (PPRE). The DNA microarray analysis was used to characterize the transcriptome of the mifepristone-induced adipocytes. In vivo adipogenic effect of mifepristone was examined in mice. RESULTS Mifepristone not only enhanced adipocyte differentiation induced by the conventional protocol consisting of insulin, dexamethasone and 3-isobutyl-1-methylxanthine but also induced adipocyte differentiation alone, as evidenced by lipid droplets formation and induction of the expression of adiponectin and Fabp4. These effects were inhibited by an adiponectin-neutralizing antibody and a PPARγ antagonist. Mifepristone activated the promoter activity of PPRE in a manner sensitive to PPARγ antagonist. A principal component analysis (PCA) of DNA microarray data revealed that the mifepristone-induced adipocytes represent some characteristics of the in situ adipocytes in normal adipose tissues to a greater extent than those induced by the conventional protocol. Mifepristone administration induced an increase in the weight of epididymal, perirenal and gluteofemoral adipose tissues. CONCLUSIONS Mifepristone alone is capable of inducing adipocyte differentiation in 3T3-L1 cells and adipogenesis in vivo. PPARγ plays a critical role in the mifepristone-induced adipocyte differentiation. Mifepristone-induced adipocytes are closer to the in situ adipocytes than those induced by the conventional protocol. The present study proposes a single treatment with mifepristone as a novel protocol to induce more physiologically relevant adipocytes in 3T3-L1 cells than the conventional protocol.
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Affiliation(s)
- Takeshi Hashimoto
- Department of Cardiovascular Physiology, Faculty of Medicine, Kagawa University, 1750-1 Miki-Cho, Kita-Gun, Kagawa, 761-0793, Japan.
| | - Katsuya Hirano
- Department of Cardiovascular Physiology, Faculty of Medicine, Kagawa University, 1750-1 Miki-Cho, Kita-Gun, Kagawa, 761-0793, Japan
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Nielsen MB, Çolak Y, Benn M, Mason A, Burgess S, Nordestgaard BG. Plasma adiponectin levels and risk of heart failure, atrial fibrillation, aortic valve stenosis, and myocardial infarction: large-scale observational and Mendelian randomization evidence. Cardiovasc Res 2024; 120:95-107. [PMID: 37897683 PMCID: PMC10898934 DOI: 10.1093/cvr/cvad162] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Grants] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 02/10/2023] [Revised: 09/07/2023] [Accepted: 09/23/2023] [Indexed: 10/30/2023] Open
Abstract
AIMS Adiponectin may play an important protective role in heart failure and associated cardiovascular diseases. We hypothesized that plasma adiponectin is associated observationally and causally, genetically with risk of heart failure, atrial fibrillation, aortic valve stenosis, and myocardial infarction. METHODS AND RESULTS In the Copenhagen General Population Study, we examined 30 045 individuals with plasma adiponectin measurements observationally and 96 903 individuals genetically in one-sample Mendelian randomization analyses using five genetic variants explaining 3% of the variation in plasma adiponectin. In the HERMES, UK Biobank, The Nord-Trøndelag Health Study (HUNT), deCODE, the Michigan Genomics Initiative (MGI), DiscovEHR, and the AFGen consortia, we performed two-sample Mendelian randomization analyses in up to 1 030 836 individuals using 12 genetic variants explaining 14% of the variation in plasma adiponectin.In observational analyses modelled linearly, a 1 unit log-transformed higher plasma adiponectin was associated with a hazard ratio of 1.51 (95% confidence interval: 1.37-1.66) for heart failure, 1.63 (1.50-1.78) for atrial fibrillation, 1.21 (1.03-1.41) for aortic valve stenosis, and 1.03 (0.93-1.14) for myocardial infarction; levels above the median were also associated with an increased risk of myocardial infarction, and non-linear U-shaped associations were more apparent for heart failure, aortic valve stenosis, and myocardial infarction in less-adjusted models. Corresponding genetic, causal risk ratios were 0.92 (0.65-1.29), 0.87 (0.68-1.12), 1.55 (0.87-2.76), and 0.93 (0.67-1.30) in one-sample Mendelian randomization analyses, and no significant associations were seen for non-linear one-sample Mendelian randomization analyses; corresponding causal risk ratios were 0.99 (0.89-1.09), 1.00 (0.92-1.08), 1.01 (0.79-1.28), and 0.99 (0.86-1.13) in two-sample Mendelian randomization analyses, respectively. CONCLUSION Observationally, elevated plasma adiponectin was associated with an increased risk of heart failure, atrial fibrillation, aortic valve stenosis, and myocardial infarction. However, genetic evidence did not support causality for these associations.
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Affiliation(s)
- Maria Booth Nielsen
- Department of Clinical Biochemistry, Copenhagen University Hospital—Herlev and Gentofte, Borgmester Ib Juuls Vej 73, Entrance 7, 4. Floor, M3, DK-2730 Herlev, Copenhagen, Denmark
- The Copenhagen General Population Study, Copenhagen University Hospital—Herlev and Gentofte, Borgmester Ib Juuls Vej 73, Entrance 7, 4. Floor, M3, DK-2730 Herlev, Copenhagen, Denmark
- Department of Clinical Medicine, Faculty of Health and Medical Sciences, University of Copenhagen, Blegdamsvej 3B, DK-2200 Copenhagen N, Copenhagen, Denmark
| | - Yunus Çolak
- The Copenhagen General Population Study, Copenhagen University Hospital—Herlev and Gentofte, Borgmester Ib Juuls Vej 73, Entrance 7, 4. Floor, M3, DK-2730 Herlev, Copenhagen, Denmark
- Department of Clinical Medicine, Faculty of Health and Medical Sciences, University of Copenhagen, Blegdamsvej 3B, DK-2200 Copenhagen N, Copenhagen, Denmark
- Department of Respiratory Medicine, Copenhagen University Hospital—Herlev and Gentofte, Copenhagen, Denmark
| | - Marianne Benn
- The Copenhagen General Population Study, Copenhagen University Hospital—Herlev and Gentofte, Borgmester Ib Juuls Vej 73, Entrance 7, 4. Floor, M3, DK-2730 Herlev, Copenhagen, Denmark
- Department of Clinical Medicine, Faculty of Health and Medical Sciences, University of Copenhagen, Blegdamsvej 3B, DK-2200 Copenhagen N, Copenhagen, Denmark
- Department of Clinical Biochemistry, Copenhagen University Hospital—Rigshospitalet, Copenhagen, Denmark
| | - Amy Mason
- Medical Research Council Biostatistics Unit, University of Cambridge, Cambridge, United Kingdom
- British Heart Foundation Cardiovascular Epidemiology Unit, Department of Public Health and Primary Care, University of Cambridge, Cambridge, United Kingdom
- Heart and Lung Research Institute, University of Cambridge, Cambridge, United Kingdom
| | - Stephen Burgess
- Medical Research Council Biostatistics Unit, University of Cambridge, Cambridge, United Kingdom
- British Heart Foundation Cardiovascular Epidemiology Unit, Department of Public Health and Primary Care, University of Cambridge, Cambridge, United Kingdom
- Heart and Lung Research Institute, University of Cambridge, Cambridge, United Kingdom
| | - Børge Grønne Nordestgaard
- Department of Clinical Biochemistry, Copenhagen University Hospital—Herlev and Gentofte, Borgmester Ib Juuls Vej 73, Entrance 7, 4. Floor, M3, DK-2730 Herlev, Copenhagen, Denmark
- The Copenhagen General Population Study, Copenhagen University Hospital—Herlev and Gentofte, Borgmester Ib Juuls Vej 73, Entrance 7, 4. Floor, M3, DK-2730 Herlev, Copenhagen, Denmark
- Department of Clinical Medicine, Faculty of Health and Medical Sciences, University of Copenhagen, Blegdamsvej 3B, DK-2200 Copenhagen N, Copenhagen, Denmark
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Hafiane A. Adiponectin-mediated regulation of the adiponectin cascade in cardiovascular disease: Updates. Biochem Biophys Res Commun 2024; 694:149406. [PMID: 38134479 DOI: 10.1016/j.bbrc.2023.149406] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 08/08/2023] [Revised: 12/03/2023] [Accepted: 12/18/2023] [Indexed: 12/24/2023]
Abstract
The endocrine function of white adipose tissue is characterized by the synthesis of one its main hormones: adiponectin. Although the biological role of adiponectin has not been fully defined, clinical and experimental observations have shown that low plasma concentrations of adiponectin participate in the prevalence of insulin resistance and cardiovascular diseases, mainly in obese patients. Adiponectin also exerts its effects on the heart and blood vessels, thereby influencing their physiology. Studying the effects of adiponectin presents some complexities, primarily due to potential cross-interactions and interference with other pathways, such as the AdipoR1/R2 pathways. Under optimal conditions, the activation of the adiponectin cascade may involve signals such as AMPK and PPARα. Interestingly, these pathways may trigger similar responses, such as fatty acid oxidation. Understanding the downstream effectors of these pathways is crucial to comprehend the extent to which adiponectin signaling impacts metabolism. In this review, the aim is to explore the current mechanisms that regulate the adiponectin pathways. Additionally, updates on the major downstream factors involved in adiponectin signaling are provided, specifically in relation to metabolic syndrome and atherosclerosis.
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Affiliation(s)
- Anouar Hafiane
- Research Institute, McGill University Health Center, Montreal, QC, Canada.
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12
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Zakaria Z, Othman ZA, Nna VU, Mohamed M. The promising roles of medicinal plants and bioactive compounds on hepatic lipid metabolism in the treatment of non-alcoholic fatty liver disease in animal models: molecular targets. Arch Physiol Biochem 2023; 129:1262-1278. [PMID: 34153200 DOI: 10.1080/13813455.2021.1939387] [Citation(s) in RCA: 2] [Impact Index Per Article: 1.0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 09/11/2020] [Accepted: 06/01/2021] [Indexed: 12/13/2022]
Abstract
Imbalance in hepatic lipid metabolism can lead to an abnormal triglycerides deposition in the hepatocytes which can cause non-alcoholic fatty liver disease (NAFLD). Four main mechanisms responsible for regulating hepatic lipid metabolism are fatty acid uptake, de novo lipogenesis, lipolysis and fatty acid oxidation. Controlling the expression of transcription factors at molecular level plays a crucial role in NAFLD management. This paper reviews various medicinal plants and their bioactive compounds emphasising mechanisms involved in hepatic lipid metabolism, other important NAFLD pathological features, and their promising roles in managing NAFLD through regulating key transcription factors. Although there are many medicinal plants popularly investigated for NAFLD treatment, there is still little information and scientific evidence available and there has been no research on clinical trials scrutinised on this matter. This review also aims to provide molecular information of medicinal plants in NALFD treatment that might have potentials for future scientifically controlled studies.
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Affiliation(s)
- Zaida Zakaria
- Department of Physiology, School of Medical Sciences, Health Campus, Universiti Sains Malaysia, Kelantan, Malaysia
| | - Zaidatul Akmal Othman
- Department of Physiology, School of Medical Sciences, Health Campus, Universiti Sains Malaysia, Kelantan, Malaysia
- Unit of Physiology, Faculty of Medicine, Universiti Sultan Zainal Abidin, Kuala Terengganu, Malaysia
| | - Victor Udo Nna
- Department of Physiology, Faculty of Basic Medical Sciences, College of Medical Sciences, University of Calabar, Calabar, Nigeria
| | - Mahaneem Mohamed
- Department of Physiology, School of Medical Sciences, Health Campus, Universiti Sains Malaysia, Kelantan, Malaysia
- Unit of Integrative Medicine, School of Medical Sciences, Health Campus, Universiti Sains Malaysia, Kelantan, Malaysia
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Al Zein M, Zein O, Diab R, Dimachkie L, Sahebkar A, Al-Asmakh M, Kobeissy F, Eid AH. Intermittent fasting favorably modulates adipokines and potentially attenuates atherosclerosis. Biochem Pharmacol 2023; 218:115876. [PMID: 37871879 DOI: 10.1016/j.bcp.2023.115876] [Citation(s) in RCA: 8] [Impact Index Per Article: 4.0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 09/19/2023] [Revised: 10/19/2023] [Accepted: 10/20/2023] [Indexed: 10/25/2023]
Abstract
Adipose tissue is now recognized as an endocrine organ that secretes bioactive molecules called adipokines. These biomolecules regulate key physiological functions, including insulin sensitivity, energy metabolism, appetite regulation, endothelial function and immunity. Dysregulated secretion of adipokines is intimately associated with obesity, and translates into increased risk of obesity-related cardiovasculo-metabolic diseases. In particular, emerging evidence suggests that adipokine imbalance contributes to the pathogenesis of atherosclerosis. One of the promising diet regimens that is beneficial in the fight against obesity and cardiometabolic disorders is intermittent fasting (IF). Indeed, IF robustly suppresses inflammation, meditates weight loss and mitigates many aspects of the cardiometabolic syndrome. In this paper, we review the main adipokines and their role in atherosclerosis, which remains a major contributor to cardiovascular-associated morbidity and mortality. We further discuss how IF can be employed as an effective management modality for obesity-associated atherosclerosis. By exploring a plethora of the beneficial effects of IF, particularly on inflammatory markers, we present IF as a possible intervention to help prevent atherosclerosis.
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Affiliation(s)
- Mohammad Al Zein
- Faculty of Medical Sciences, Lebanese University, Hadath, Beirut, Lebanon
| | - Omar Zein
- Faculty of Medicine, American University of Beirut, Beirut, Lebanon
| | - Rawan Diab
- Faculty of Medicine, American University of Beirut, Beirut, Lebanon
| | - Lina Dimachkie
- Faculty of Medicine, American University of Beirut, Beirut, Lebanon
| | - Amirhossein Sahebkar
- Biotechnology Research Center, Pharmaceutical Technology Institute, Mashhad University of Medical Sciences, Mashhad, Iran; Applied Biomedical Research Center, Mashhad University of Medical Sciences, Mashhad, Iran
| | - Maha Al-Asmakh
- Department of Biomedical Sciences, College of Health Sciences, QU Health, Qatar University, Doha, Qatar; Biomedical Research Center, Qatar University, Doha, Qatar
| | - Firas Kobeissy
- Department of Neurobiology and Neuroscience, Morehouse School of Medicine, Atlanta, GA, USA
| | - Ali H Eid
- Department of Basic Medical Sciences, College of Medicine, QU Health, Qatar University, Doha, Qatar.
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Mengi Çelik Ö, Köksal E, Aktürk M. Time-restricted eating (16/8) and energy-restricted diet: effects on diet quality, body composition and biochemical parameters in healthy overweight females. BMC Nutr 2023; 9:97. [PMID: 37559145 PMCID: PMC10410965 DOI: 10.1186/s40795-023-00753-6] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 01/12/2023] [Accepted: 07/26/2023] [Indexed: 08/11/2023] Open
Abstract
BACKGROUND Time-restricted eating (TRE) is a current popular dietary strategy for noncommunicable diseases. However, studies demonstrated contradictory results for it and in all dietary strategies, diet quality is an the important part of the well-being. Our study aimed to investigate the effect of TRE and energy-restricted diet (ERD) on the nutritional status and diet quality of individuals. METHODS This pilot study was completed 23 healthy overweight female. Anthropometric and body composition measurements of individuals were taken. The energy expenditure was measured using indirect calorimetry. Blood pressure and heart rate measurements were made. Biochemical parameters were evaluated and food consumption were taken. The quality of dietary intake was assessed using the Healthy Eating Index (HEI) -2015. The physical activity levels of the individuals were estimated using the physical activity record. The Statistical Package for the Social Sciences (version 22.0) software was used for all analyses. A p-value of less than 0.05 was considered to be statistically significant. RESULTS After 8 weeks of intervention, while no change was observed in the diet quality of the individuals in the TRE group (p > 0.05), a significant increase was found in the diet quality score of the individuals in the ERD group (p < 0.05). There was a 3.2% and 5.5% decrease in body weight of individuals in the TRE and ERD groups, respectively (p < 0.05). While no significant change was observed in the body fat percentage of individuals in the TRE group (p > 0.05), a 7.1% decrease was observed in the ERD group (p < 0.05). A statistically significant decrease was found in the total cholesterol (3.7%) in the ERD group, and in the total cholesterol (6.7%) and low density lipoprotein cholesterol (LDL-C) (6.5%) in the TRE group. In addition, a statistically significant increase was found in adiponectin (77.3%) and total antioxidant status (TAS) (13.2%) in the ERD group. CONCLUSION Energy-restricted diet yielded better results in weight loss and improvement of body composition and diet quality compared to TRE. Also, a decrease in total cholesterol level was found in the ERD group. However, more studies should be done with longer follow-ups and high sample sizes are very important in terms of creating public health-based recommendations.
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Affiliation(s)
- Özge Mengi Çelik
- Faculty of Health Sciences, Department of Nutrition and Dietetics, University of Health Sciences, Ankara, Turkey.
| | - Eda Köksal
- Faculty of Health Sciences, Department of Nutrition and Dietetics, Gazi University, Ankara, Turkey
| | - Müjde Aktürk
- Faculty of Medicine, Department of Endocrinology, Gazi University, Ankara, Turkey
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15
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Crocker CE, Sharmeen R, Tran TT, Khan AM, Li W, Alcorn JL. Surfactant protein a attenuates generalized and localized neuroinflammation in neonatal mice. Brain Res 2023; 1807:148308. [PMID: 36871846 PMCID: PMC10065943 DOI: 10.1016/j.brainres.2023.148308] [Citation(s) in RCA: 1] [Impact Index Per Article: 0.5] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Grants] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 12/14/2022] [Revised: 02/24/2023] [Accepted: 02/28/2023] [Indexed: 03/06/2023]
Abstract
Surfactant protein A (SP-A) has important roles in innate immunity and modulation of pulmonary and extrapulmonary inflammation. Given SP-A has been detected in rat and human brain, we sought to determine if SP-A has a role in modulating inflammation in the neonatal mouse brain. Neonatal wildtype (WT) and SP-A-deficient (SP-A-/-) mice were subjected to three models of brain inflammation: systemic sepsis, intraventricular hemorrhage (IVH) and hypoxic-ischemic encephalopathy (HIE). Following each intervention, RNA was isolated from brain tissue and expression of cytokine and SP-A mRNA was determined by real-time quantitative RT-PCR analysis. In the sepsis model, expression of most cytokine mRNAs was significantly increased in brains of WT and SP-A-/- mice with significantly greater expression of all cytokine mRNA levels in SP-A-/- mice compared to WT. In the IVH model, expression of all cytokine mRNAs was significantly increased in WT and SP-A-/- mice and levels of most cytokine mRNAs were significantly increased in SP-A-/- mice compared to WT. In the HIE model, only TNF-α mRNA levels were significantly increased in WT brain tissue while all pro-inflammtory cytokine mRNAs were significantly increased in SP-A-/- mice, and all pro-inflammatory cytokine mRNA levels were significantly higher in SP-A-/- mice compared to WT. SP-A mRNA was not detectable in brain tissue of adult WT mice nor in WT neonates subjected to these models. These results suggest that SP-A-/- neonatal mice subjected to models of neuroinflammation are more susceptible to both generalized and localized neuroinflammation compared to WT mice, thus supporting the hypothesis that SP-A attenuates inflammation in neonatal mouse brain.
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Affiliation(s)
- Caroline E Crocker
- Division of Neonatology, Department of Pediatrics, McGovern Medical School, University of Texas Health Science Center at Houston, Houston, TX 77030, USA
| | - Romana Sharmeen
- Department of Neurology, McGovern Medical School, University of Texas Health Science Center at Houston, Houston, TX 77030, USA
| | - Thu T Tran
- Division of Neonatology, Department of Pediatrics, McGovern Medical School, University of Texas Health Science Center at Houston, Houston, TX 77030, USA
| | - Amir M Khan
- Division of Neonatology, Department of Pediatrics, McGovern Medical School, University of Texas Health Science Center at Houston, Houston, TX 77030, USA
| | - Wen Li
- Division of Clinical and Translational Sciences, Department of Internal Medicine, the University of Texas McGovern Medical School at Houston, Houston, TX 77030, USA; Biostatistics/Epidemiology/Research Design Component, Center for Clinical and Translational Sciences, University of Texas Health Science Center at Houston, Houston, TX 77030, USA
| | - Joseph L Alcorn
- Division of Neonatology, Department of Pediatrics, McGovern Medical School, University of Texas Health Science Center at Houston, Houston, TX 77030, USA; Pediatric Research Center, Department of Pediatrics, McGovern Medical School, University of Texas Health Science Center at Houston, Houston, TX 77030, USA.
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Peng J, Chen Q, Wu C. The role of adiponectin in cardiovascular disease. Cardiovasc Pathol 2023; 64:107514. [PMID: 36634790 DOI: 10.1016/j.carpath.2022.107514] [Citation(s) in RCA: 27] [Impact Index Per Article: 13.5] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 08/27/2022] [Revised: 12/14/2022] [Accepted: 12/16/2022] [Indexed: 01/11/2023] Open
Abstract
Cardiovascular disease (CVD) is a common disease that seriously threatens the health of human beings, especially middle-aged and elderly people over 50 years old. It has the characteristics of high prevalence, high disability rate and high mortality rate. Previous studies have shown that adiponectin has therapeutic effects on a variety of CVDs. As a key adipokine, adiponectin, is an abundant peptide-regulated hormone that is mainly released by adipocytes and cardiomyocytes, as well as endothelial and skeletal cells. Adiponectin can protect against CVD by improving lipid metabolism, protecting vascular endothelial cells and inhibiting foam cell formation and vascular smooth muscle cell proliferation. Further investigation of the molecular and cellular mechanisms underlying the adiponectin system may provide new ideas for the treatment of CVD. Herein, this review aims to describe the structure and function of adiponectin and adiponectin receptors, introduce the function of adiponectin in the protection of cardiovascular disease and analyze the potential use and clinical significance of this hormone in the protection and treatment of cardiovascular disease, which shows that adiponectin can be expected to become a new therapeutic target and biomarker for the diagnosis and treatment of CVD.
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Affiliation(s)
- Jin Peng
- Clinical Medical Research Center, Xinqiao Hospital, Army Medical University, Chongqing, China
| | - Qian Chen
- Clinical Medical Research Center, Xinqiao Hospital, Army Medical University, Chongqing, China
| | - Chuncao Wu
- Insititution of Chinese Materia Medica Preparation, Chongqing Hospital of Traditional Chinese Medicine, Chongqing, China.
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Jehn S, Roggel A, Dykun I, Balcer B, Al-Rashid F, Totzeck M, Risse J, Kill C, Rassaf T, Mahabadi AA. Epicardial adipose tissue and obstructive coronary artery disease in acute chest pain: the EPIC-ACS study. EUROPEAN HEART JOURNAL OPEN 2023; 3:oead041. [PMID: 37143611 PMCID: PMC10152391 DOI: 10.1093/ehjopen/oead041] [Citation(s) in RCA: 8] [Impact Index Per Article: 4.0] [Reference Citation Analysis] [Abstract] [Key Words] [Grants] [Track Full Text] [Download PDF] [Figures] [Subscribe] [Scholar Register] [Received: 01/03/2023] [Revised: 03/01/2023] [Accepted: 04/14/2023] [Indexed: 05/06/2023]
Abstract
Aims We tested the hypothesis that epicardial adipose tissue (EAT) quantification improves the prediction of the presence of obstructive coronary artery disease (CAD) in patients presenting with acute chest pain to the emergency department. Methods and results Within this prospective observational cohort study, we included 657 consecutive patients (mean age 58.06 ± 18.04 years, 53% male) presenting to the emergency department with acute chest pain suggestive of acute coronary syndrome between December 2018 and August 2020. Patients with ST-elevation myocardial infarction, haemodynamic instability, or known CAD were excluded. As part of the initial workup, we performed bedside echocardiography for quantification of EAT thickness by a dedicated study physician, blinded to all patient characteristics. Treating physicians remained unaware of the results of the EAT assessment. The primary endpoint was defined as the presence of obstructive CAD, as detected in subsequent invasive coronary angiography. Patients reaching the primary endpoint had significantly more EAT than patients without obstructive CAD (7.90 ± 2.56 mm vs. 3.96 ± 1.91 mm, P < 0.0001). In a multivariable regression analysis, a 1 mm increase in EAT thickness was associated with a nearby two-fold increased odds of the presence of obstructive CAD [1.87 (1.64-2.12), P < 0.0001]. Adding EAT to a multivariable model of the GRACE score, cardiac biomarkers and traditional risk factors significantly improved the area under the receiver operating characteristic curve (0.759-0.901, P < 0.0001). Conclusion Epicardial adipose tissue strongly and independently predicts the presence of obstructive CAD in patients presenting with acute chest pain to the emergency department. Our results suggest that the assessment of EAT may improve diagnostic algorithms of patients with acute chest pain.
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Affiliation(s)
- Stefanie Jehn
- The West German Heart and Vascular Center Essen, Department of Cardiology and Vascular Medicine, University Hospital Essen, Hufelandstr. 55, 45147 Essen, Germany
| | - Anja Roggel
- The West German Heart and Vascular Center Essen, Department of Cardiology and Vascular Medicine, University Hospital Essen, Hufelandstr. 55, 45147 Essen, Germany
| | - Iryna Dykun
- The West German Heart and Vascular Center Essen, Department of Cardiology and Vascular Medicine, University Hospital Essen, Hufelandstr. 55, 45147 Essen, Germany
| | - Bastian Balcer
- The West German Heart and Vascular Center Essen, Department of Cardiology and Vascular Medicine, University Hospital Essen, Hufelandstr. 55, 45147 Essen, Germany
| | - Fadi Al-Rashid
- The West German Heart and Vascular Center Essen, Department of Cardiology and Vascular Medicine, University Hospital Essen, Hufelandstr. 55, 45147 Essen, Germany
| | - Matthias Totzeck
- The West German Heart and Vascular Center Essen, Department of Cardiology and Vascular Medicine, University Hospital Essen, Hufelandstr. 55, 45147 Essen, Germany
| | - Joachim Risse
- Center of Emergency Medicine, University Hospital Essen, Hufelandstr. 55, 45147 Essen, Germany
| | - Clemens Kill
- Center of Emergency Medicine, University Hospital Essen, Hufelandstr. 55, 45147 Essen, Germany
| | - Tienush Rassaf
- The West German Heart and Vascular Center Essen, Department of Cardiology and Vascular Medicine, University Hospital Essen, Hufelandstr. 55, 45147 Essen, Germany
| | - Amir A Mahabadi
- Corresponding author. Tel: +49 (0)201/723 84822, Fax: +49 (0)201/723 5401,
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Roy PK, Islam J, Lalhlenmawia H. Prospects of potential adipokines as therapeutic agents in obesity-linked atherogenic dyslipidemia and insulin resistance. Egypt Heart J 2023; 75:24. [PMID: 37014444 PMCID: PMC10073393 DOI: 10.1186/s43044-023-00352-7] [Citation(s) in RCA: 7] [Impact Index Per Article: 3.5] [Reference Citation Analysis] [Abstract] [Key Words] [Journal Information] [Subscribe] [Scholar Register] [Received: 05/27/2022] [Accepted: 03/28/2023] [Indexed: 04/05/2023] Open
Abstract
BACKGROUND In normal circumstances, AT secretes anti-inflammatory adipokines (AAKs) which regulates lipid metabolism, insulin sensitivity, vascular hemostasis, and angiogenesis. However, during obesity AT dysfunction occurs and leads to microvascular imbalance and secretes several pro-inflammatory adipokines (PAKs), thereby favoring atherogenic dyslipidemia and insulin resistance. Literature suggests decreased levels of circulating AAKs and increased levels of PAKs in obesity-linked disorders. Importantly, AAKs have been reported to play a vital role in obesity-linked metabolic disorders mainly insulin resistance, type-2 diabetes mellitus and coronary heart diseases. Interestingly, AAKs counteract the microvascular imbalance in AT and exert cardioprotection via several signaling pathways such as PI3-AKT/PKB pathway. Although literature reviews have presented a number of investigations detailing specific pathways involved in obesity-linked disorders, literature concerning AT dysfunction and AAKs remains sketchy. In view of the above, in the present contribution an effort has been made to provide an insight on the AT dysfunction and role of AAKs in modulating the obesity and obesity-linked atherogenesis and insulin resistance. MAIN BODY "Obesity-linked insulin resistance", "obesity-linked cardiometabolic disease", "anti-inflammatory adipokines", "pro-inflammatory adipokines", "adipose tissue dysfunction" and "obesity-linked microvascular dysfunction" are the keywords used for searching article. Google scholar, Google, Pubmed and Scopus were used as search engines for the articles. CONCLUSIONS This review offers an overview on the pathophysiology of obesity, management of obesity-linked disorders, and areas in need of attention such as novel therapeutic adipokines and their possible future perspectives as therapeutic agents.
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Affiliation(s)
- Probin Kr Roy
- Department of Pharmacy, Regional Institute of Paramedical and Nursing Sciences (RIPANS), Aizawl, Mizoram, 796017, India.
| | - Johirul Islam
- Coromandel International Limited, Hyderabad, Telangana, 500101, India
| | - Hauzel Lalhlenmawia
- Department of Pharmacy, Regional Institute of Paramedical and Nursing Sciences (RIPANS), Aizawl, Mizoram, 796017, India
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Hepatokines and Adipokines in Metabolic Syndrome. ANNALS OF THE NATIONAL ACADEMY OF MEDICAL SCIENCES (INDIA) 2023. [DOI: 10.1055/s-0042-1760087] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 02/18/2023] Open
Abstract
AbstractHepatokines and adipokines are secretory proteins derived from hepatocytes and adipocytes, respectively. These proteins play a main role in the pathogenesis of metabolic syndrome (MetS), characterized by obesity, dysglycemia, insulin resistance, dyslipidemia, and hypertension. Adipose tissue and liver are important endocrine organs because they regulate metabolic homeostasis as well as inflammation because they secrete adipokines and hepatokines, respectively. These adipokines and hepatokines communicate their action through different autocrine, paracrine and endocrine pathways. Liver regulates systemic homeostasis and also glucose and lipid metabolism through hepatokines. Dysregulation of hepatokines can lead to progression toward MetS, type 2 diabetes (T2D), inflammation, hypertension, and other diseases. Obesity is now a worldwide epidemic. Increasing cases of obesity and obesity-associated metabolic syndrome has brought the focus on understanding the biology of adipocytes and the mechanisms occurring in adipose tissue of obese individuals. A lot of facts are now available on adipose tissue as well. Adipose tissue is now given the status of an endocrine organ. Recent evidence indicates that obesity contributes to systemic metabolic dysfunction. Adipose tissue plays a significant role in systemic metabolism by communicating with other central and peripheral organs via the production and secretion of a group of proteins known as adipokines. Adipokine levels regulate metabolic state of our body and are potent enough to have a direct impact upon energy homeostasis and systemic metabolism. Dysregulation of adipokines contribute to obesity, T2D, hypertension and several other pathological changes in various organs. This makes characterization of hepatokines and adipokines extremely important to understand the pathogenesis of MetS. Hepatokines such as fetuin-A and leukocyte cell-derived chemotaxin 2, and adipokines such as resistin, leptin, TNF-α, and adiponectin are some of the most studied proteins and they can modulate the manifestations of MetS. Detailed insight into the function and mechanism of these adipokines and hepatokines in the pathogenesis of MetS can show the path for devising better preventative and therapeutic strategies against this present-day pandemic.
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Felipe LA, Bachi ALL, Oliveira MC, Moreira SMBP, Afonso JPR, Lino MEM, Paixão V, Silva CHM, Vieira RP, Vencio S, Jirjos EI, Malheiros CA, Insalaco G, Júnior WRF, Oliveira LVF. Effects of Roux-en-Y gastric bypass on the metabolic profile and systemic inflammatory status of women with metabolic syndrome: randomized controlled clinical trial. Diabetol Metab Syndr 2023; 15:19. [PMID: 36788619 PMCID: PMC9930348 DOI: 10.1186/s13098-023-00986-2] [Citation(s) in RCA: 3] [Impact Index Per Article: 1.5] [Reference Citation Analysis] [Abstract] [Key Words] [Grants] [Track Full Text] [Figures] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 07/06/2022] [Accepted: 01/25/2023] [Indexed: 02/16/2023] Open
Abstract
BACKGROUND Obesity remains a public health problem worldwide. The high prevalence of this condition in the population raises further concerns, considering that comorbidities are often associated with obesity. Among the comorbidities closely associated with obesity, metabolic syndrome (MS) is particularly important, which potentially increases the risk of manifestation of other disorders, such as the prothrombotic and systemic pro-inflammatory states. METHODS A randomized, controlled clinical trial was performed involving female patients (n = 32) aged between 18 and 65 years, with a clinical diagnosis of MS, with severe obesity undergoing Roux-en-Y gastric bypass (RYGB). The study design followed the Consolidated Standards of Reporting Trials statement (CONSORT). Lipid profile, blood glucose and adipokines (adiponectin, leptin, and resistin) and (cytokines IL-1β, IL-6, IL-17, IL-23, and TNF-α) in blood plasma samples were evaluated before and six months after RYGB. RESULTS Patients undergoing RYGB (BSG) showed a significant improvement from preoperative grade III obesity to postoperative grade I obesity. The results showed that while HDL levels increased, the other parameters showed a significant reduction in their postoperative values when compared not only to the values observed before surgery in the BSG group, but also to the values obtained in the control group (CG). As for systemic inflammatory markers adiponectin, leptin, resistin, IL-1β, IL-6, IL-17, IL-23 and TNF- α it was observed that the levels of resistin and IL-17 in the second evaluation increased significantly when compared to the levels observed in the first evaluation in the CG. In the BSG group, while the levels of adiponectin increased, the levels of the other markers showed significant reductions in the postoperative period, in relation to the respective preoperative levels. The analysis of Spearman's correlation coefficient showed a significant positive correlation between IL-17 and IL-23 in the preoperative period, significant positive correlations between TNF-α and IL-6, TNF-α and IL-17, IL-6 and IL-17, and IL-17 and IL-23 were observed postoperatively. CONCLUSIONS According to our results, the reduction of anthropometric measurements induced by RYGB, significantly improves not only the plasma biochemical parameters (lipid profile and glycemia), but also the systemic inflammatory status of severely obese patients with MS. Trials registration NCT02409160.
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Affiliation(s)
- Lucenda A Felipe
- Post-Graduation Program in Health Sciences, Santa Casa of Sao Paulo Medical School, Sao Paulo, SP, 01221-010, Brazil
| | - André L L Bachi
- Post-Graduation Program in Health Sciences, Santo Amaro University (UNISA), São Paulo, SP, Brazil
| | - Miriã C Oliveira
- Human Movement and Rehabilitation Post Graduation Program, Evangelical University of Goiás (UniEVANGELICA), Anápolis, GO, Brazil
| | - Sandra M B P Moreira
- Post-Graduation Program in Health Sciences, Santa Casa of Sao Paulo Medical School, Sao Paulo, SP, 01221-010, Brazil
| | - João Pedro R Afonso
- Human Movement and Rehabilitation Post Graduation Program, Evangelical University of Goiás (UniEVANGELICA), Anápolis, GO, Brazil
| | - Maria E M Lino
- Scientific Initiation Program, Evangelical University of Goiás, (UniEVANGELICA), Anápolis, GO, Brazil
| | - Vitória Paixão
- Department of Otorhinolaryngology, ENT Lab, Federal University of São Paulo (UNIFESP), São Paulo, SP, 04021-001, Brazil
| | - Carlos H M Silva
- Human Movement and Rehabilitation Post Graduation Program, Evangelical University of Goiás (UniEVANGELICA), Anápolis, GO, Brazil
| | - Rodolfo P Vieira
- Human Movement and Rehabilitation Post Graduation Program, Evangelical University of Goiás (UniEVANGELICA), Anápolis, GO, Brazil
| | - Sergio Vencio
- Institute of Pharmaceutical Sciences, Goiania, (GO), Brazil
| | - Elias I Jirjos
- Post-Graduation Program in Health Sciences, Santa Casa of Sao Paulo Medical School, Sao Paulo, SP, 01221-010, Brazil
| | - Carlos A Malheiros
- Post-Graduation Program in Health Sciences, Santa Casa of Sao Paulo Medical School, Sao Paulo, SP, 01221-010, Brazil
| | - Giuseppe Insalaco
- Institute for Biomedical Research and Innovation, National Research Council of Italy (CNR), 90146, Palermo, Italy
| | - Wilson R Freitas Júnior
- Post-Graduation Program in Health Sciences, Santa Casa of Sao Paulo Medical School, Sao Paulo, SP, 01221-010, Brazil
| | - Luis V F Oliveira
- Human Movement and Rehabilitation Post Graduation Program, Evangelical University of Goiás (UniEVANGELICA), Anápolis, GO, Brazil.
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21
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Iwaki M, Kobayashi T, Nogami A, Saito S, Nakajima A, Yoneda M. Impact of Sarcopenia on Non-Alcoholic Fatty Liver Disease. Nutrients 2023; 15:nu15040891. [PMID: 36839249 PMCID: PMC9965462 DOI: 10.3390/nu15040891] [Citation(s) in RCA: 28] [Impact Index Per Article: 14.0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 12/30/2022] [Revised: 02/07/2023] [Accepted: 02/08/2023] [Indexed: 02/12/2023] Open
Abstract
With the increasing incidence of non-alcoholic fatty liver disease (NAFLD) and the aging of the population, sarcopenia is attracting attention as one of the pathological conditions involved in the development and progression of NAFLD. In NAFLD, sarcopenia is closely associated with insulin resistance and results from the atrophy of skeletal muscle, an insulin target organ. In addition, inflammatory cytokines that promote skeletal muscle protein breakdown, low adiponectin levels leading to decreased insulin sensitivity, and hyperleptinemia are also involved in NAFLD pathogenesis. The presence of sarcopenia is a prognostic factor and increases the risk of mortality in patients with cirrhosis and post-treatment liver cancer. Sarcopenia, the presence of which mainly occurs due to decreased muscle mass, combined with increased visceral fat, can lead to sarcopenia-associated obesity, which increases the risk of NASH, liver fibrosis, and cardiovascular disease. In order to treat sarcopenia, it is necessary to properly evaluate sarcopenia status. Patients with high BMI, as in sarcopenic obesity, may improve with caloric restriction. However, inadequate oral intake may lead to further loss of muscle mass. Aerobic and resistance exercise should also be used appropriately.
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22
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Gareis NC, Rodríguez FM, Cattaneo Moreyra ML, Stassi AF, Angeli E, Etchevers L, Salvetti NR, Ortega HH, Hein GJ, Rey F. Contribution of key elements of nutritional metabolism to the development of cystic ovarian disease in dairy cattle. Theriogenology 2023; 197:209-223. [PMID: 36525860 DOI: 10.1016/j.theriogenology.2022.12.003] [Citation(s) in RCA: 3] [Impact Index Per Article: 1.5] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 08/31/2022] [Revised: 11/28/2022] [Accepted: 12/02/2022] [Indexed: 12/12/2022]
Abstract
The alteration of signaling molecules involved in the general metabolism of animals can negatively influence reproduction. In dairy cattle, the development of follicular cysts and the subsequent appearance of ovarian cystic disease (COD) often lead to decreased reproductive efficiency in the herd. The objective of this review is to summarize the contribution of relevant metabolic and nutritional sensors to the development of COD in dairy cows. In particular, we focus on the study of alterations of the insulin signaling pathway, adiponectin, and other sensors and metabolites relevant to ovarian functionality, which may be related to the development of follicular persistence and follicular formation of cysts in dairy cattle. The results of these studies support the hypothesis that systemic factors could alter the local scenario in the follicle, generating an adverse microenvironment for the resumption of ovarian activity and possibly leading to the persistence of follicles and to the development and recurrence of COD.
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Affiliation(s)
- N C Gareis
- Laboratorio de Biología Celular y Molecular Aplicada, ICiVet-Litoral (UNL-CONICET), Esperanza, Santa Fe, Argentina; Facultad de Ciencias Veterinarias - Universidad Nacional del Litoral, Esperanza, Santa Fe, Argentina
| | - F M Rodríguez
- Laboratorio de Biología Celular y Molecular Aplicada, ICiVet-Litoral (UNL-CONICET), Esperanza, Santa Fe, Argentina; Facultad de Ciencias Veterinarias - Universidad Nacional del Litoral, Esperanza, Santa Fe, Argentina
| | - M L Cattaneo Moreyra
- Laboratorio de Biología Celular y Molecular Aplicada, ICiVet-Litoral (UNL-CONICET), Esperanza, Santa Fe, Argentina
| | - A F Stassi
- Laboratorio de Biología Celular y Molecular Aplicada, ICiVet-Litoral (UNL-CONICET), Esperanza, Santa Fe, Argentina; Facultad de Ciencias Veterinarias - Universidad Nacional del Litoral, Esperanza, Santa Fe, Argentina
| | - E Angeli
- Laboratorio de Biología Celular y Molecular Aplicada, ICiVet-Litoral (UNL-CONICET), Esperanza, Santa Fe, Argentina; Facultad de Ciencias Veterinarias - Universidad Nacional del Litoral, Esperanza, Santa Fe, Argentina
| | - L Etchevers
- Laboratorio de Biología Celular y Molecular Aplicada, ICiVet-Litoral (UNL-CONICET), Esperanza, Santa Fe, Argentina; Facultad de Ciencias Veterinarias - Universidad Nacional del Litoral, Esperanza, Santa Fe, Argentina
| | - N R Salvetti
- Laboratorio de Biología Celular y Molecular Aplicada, ICiVet-Litoral (UNL-CONICET), Esperanza, Santa Fe, Argentina; Facultad de Ciencias Veterinarias - Universidad Nacional del Litoral, Esperanza, Santa Fe, Argentina
| | - H H Ortega
- Laboratorio de Biología Celular y Molecular Aplicada, ICiVet-Litoral (UNL-CONICET), Esperanza, Santa Fe, Argentina; Facultad de Ciencias Veterinarias - Universidad Nacional del Litoral, Esperanza, Santa Fe, Argentina
| | - G J Hein
- Laboratorio de Biología Celular y Molecular Aplicada, ICiVet-Litoral (UNL-CONICET), Esperanza, Santa Fe, Argentina; Centro Universitario Gálvez (CUG-UNL), Gálvez, Santa Fe, Argentina
| | - F Rey
- Laboratorio de Biología Celular y Molecular Aplicada, ICiVet-Litoral (UNL-CONICET), Esperanza, Santa Fe, Argentina; Facultad de Ciencias Veterinarias - Universidad Nacional del Litoral, Esperanza, Santa Fe, Argentina.
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23
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Pathophysiology of obesity and its associated diseases. Acta Pharm Sin B 2023. [DOI: 10.1016/j.apsb.2023.01.012] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 01/15/2023] Open
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24
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Galley JC, Singh S, Awata WMC, Alves JV, Bruder-Nascimento T. Adipokines: Deciphering the cardiovascular signature of adipose tissue. Biochem Pharmacol 2022; 206:115324. [PMID: 36309078 PMCID: PMC10509780 DOI: 10.1016/j.bcp.2022.115324] [Citation(s) in RCA: 12] [Impact Index Per Article: 4.0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Grants] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 07/15/2022] [Revised: 10/19/2022] [Accepted: 10/20/2022] [Indexed: 11/02/2022]
Abstract
Obesity and hypertension are intimately linked due to the various ways that the important cell types such as vascular smooth muscle cells (VSMC), endothelial cells (EC), immune cells, and adipocytes, communicate with one another to contribute to these two pathologies. Adipose tissue is a very dynamic organ comprised primarily of adipocytes, which are well known for their role in energy storage. More recently adipose tissue has been recognized as the largest endocrine organ because of its ability to produce a vast number of signaling molecules called adipokines. These signaling molecules stimulate specific types of cells or tissues with many adipokines acting as indicators of adipocyte healthy function, such as adiponectin, omentin, and FGF21, which show anti-inflammatory or cardioprotective effects, acting as regulators of healthy physiological function. Others, like visfatin, chemerin, resistin, and leptin are often altered during pathophysiological circumstances like obesity and lipodystrophy, demonstrating negative cardiovascular outcomes when produced in excess. This review aims to explore the role of adipocytes and their derived products as well as the impacts of these adipokines on blood pressure regulation and cardiovascular homeostasis.
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Affiliation(s)
- Joseph C. Galley
- Department of Pediatrics, University of Pittsburgh, Pittsburgh, PA, USA
- Center for Pediatrics Research in Obesity and Metabolism (CPROM), University of Pittsburgh, Pittsburgh, PA, USA
| | - Shubhnita Singh
- Department of Pediatrics, University of Pittsburgh, Pittsburgh, PA, USA
- Center for Pediatrics Research in Obesity and Metabolism (CPROM), University of Pittsburgh, Pittsburgh, PA, USA
| | - Wanessa M. C. Awata
- Department of Pediatrics, University of Pittsburgh, Pittsburgh, PA, USA
- Center for Pediatrics Research in Obesity and Metabolism (CPROM), University of Pittsburgh, Pittsburgh, PA, USA
| | - Juliano V. Alves
- Department of Pediatrics, University of Pittsburgh, Pittsburgh, PA, USA
- Center for Pediatrics Research in Obesity and Metabolism (CPROM), University of Pittsburgh, Pittsburgh, PA, USA
| | - Thiago Bruder-Nascimento
- Department of Pediatrics, University of Pittsburgh, Pittsburgh, PA, USA
- Center for Pediatrics Research in Obesity and Metabolism (CPROM), University of Pittsburgh, Pittsburgh, PA, USA
- Endocrinology Division at UPMC Children’s Hospital of Pittsburgh, University of Pittsburgh, Pittsburgh, PA, USA
- Vascular Medicine Institute (VMI), University of Pittsburgh, Pittsburgh, PA, USA
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25
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de Oliveira ASLE, Bloise G, Moltrasio C, Coelho A, Agrelli A, Moura R, Tricarico PM, Jamain S, Marzano AV, Crovella S, Cavalcanti Brandão LA. Transcriptome Meta-Analysis Confirms the Hidradenitis Suppurativa Pathogenic Triad: Upregulated Inflammation, Altered Epithelial Organization, and Dysregulated Metabolic Signaling. Biomolecules 2022; 12:1371. [PMID: 36291580 PMCID: PMC9599370 DOI: 10.3390/biom12101371] [Citation(s) in RCA: 11] [Impact Index Per Article: 3.7] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Grants] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 08/15/2022] [Revised: 09/15/2022] [Accepted: 09/20/2022] [Indexed: 11/21/2022] Open
Abstract
Hidradenitis suppurativa (HS) is an inflammatory skin condition clinically characterized by recurrent painful deep-seated nodules, abscesses, and sinus tracks in areas bearing apocrine glands, such as axillae, breasts, groins, and buttocks. Despite many recent advances, the pathophysiological landscape of HS still demands further clarification. To elucidate HS pathogenesis, we performed a meta-analysis, set analysis, and a variant calling on selected RNA-Sequencing (RNA-Seq) studies on HS skin. Our findings corroborate the HS triad composed of upregulated inflammation, altered epithelial differentiation, and dysregulated metabolism signaling. Upregulation of specific genes, such as KRT6, KRT16, serpin-family genes, and SPRR3 confirms the early involvement of hair follicles and the impairment of barrier function in HS lesioned skin. In addition, our results suggest that adipokines could be regarded as biomarkers of HS and metabolic-related disorders. Finally, the RNA-Seq variant calling identified several mutations in HS patients, suggesting potential new HS-related genes associated with the sporadic form of this disease. Overall, this study provides insights into the molecular pathways involved in HS and identifies potential HS-related biomarkers.
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Affiliation(s)
| | - Giovanna Bloise
- Department of Pathology, Federal University of Pernambuco, Recife 50670-901, Brazil
- Hospital Israelita Albert Einstein, São Paulo 05652-000, Brazil
| | - Chiara Moltrasio
- Dermatology Unit, Fondazione IRCCS Ca’ Granda Ospedale Maggiore Policlinico, 20122 Milan, Italy
- Department of Medical Surgical and Health Sciences, University of Trieste, 34137 Trieste, Italy
| | - Antonio Coelho
- Hospital Israelita Albert Einstein, São Paulo 05652-000, Brazil
| | - Almerinda Agrelli
- Laboratory of Nanostructured Materials (LMNANO), Center for Strategic Technologies Northeastern (CETENE), Av. Prof. Luís Freire, 1-Cidade Universitária, Recife 50740-545, Brazil
| | - Ronald Moura
- Department of Advanced Diagnostics, Institute for Maternal and Child Health-IRCCS “Burlo Garofolo”, 34137 Trieste, Italy
| | - Paola Maura Tricarico
- Department of Advanced Diagnostics, Institute for Maternal and Child Health-IRCCS “Burlo Garofolo”, 34137 Trieste, Italy
| | - Stéphane Jamain
- Translational Neuropsychiatry, Univ. Paris Est Créteil, Inserm, IMRB, 94010 Créteil, France
| | - Angelo Valerio Marzano
- Dermatology Unit, Fondazione IRCCS Ca’ Granda Ospedale Maggiore Policlinico, 20122 Milan, Italy
- Department of Pathophysiology and Transplantation, Università degli Studi di Milano, 20122 Milan, Italy
| | - Sergio Crovella
- Biological Science Program, Department of Biological and Environmental Sciences, College of Arts and Sciences, University of Qatar, Doha 2713, Qatar
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Pamuk F, Kantarci A. Inflammation as a link between periodontal disease and obesity. Periodontol 2000 2022; 90:186-196. [PMID: 35916870 DOI: 10.1111/prd.12457] [Citation(s) in RCA: 25] [Impact Index Per Article: 8.3] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 12/14/2022]
Abstract
Nutrition plays a critical role in the homeostatic balance, maintenance of health, and longevity. There is a close link between inflammatory diseases and nutritional health. Obesity is a severe pathological process with grave implications on several organ systems and disease processes, including type 2 diabetes, cardiovascular disease, osteoarthritis, and rheumatoid arthritis. The impact of obesity on periodontal inflammation has not been fully understood; the association between nutritional balance and periodontal inflammation is much less explored. This review is focused on the potential mechanistic links between periodontal diseases and obesity and common inflammatory activity pathways that can be pharmacologically targeted.
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Affiliation(s)
- Ferda Pamuk
- Forsyth Institute, Cambridge, Massachusetts, USA.,Department of Oral Health Sciences, University of Leuven (KU Leuven), Leuven, Belgium
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27
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Chakarov S, Blériot C, Ginhoux F. Role of adipose tissue macrophages in obesity-related disorders. J Exp Med 2022; 219:213212. [PMID: 35543703 PMCID: PMC9098652 DOI: 10.1084/jem.20211948] [Citation(s) in RCA: 44] [Impact Index Per Article: 14.7] [Reference Citation Analysis] [Abstract] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 02/06/2022] [Revised: 04/17/2022] [Accepted: 04/18/2022] [Indexed: 11/04/2022] Open
Abstract
The obesity epidemic has led researchers and clinicians to reconsider the etiology of this disease and precisely decipher its molecular mechanisms. The excessive accumulation of fat by cells, most notably adipocytes, which play a key role in this process, has many repercussions in tissue physiology. Herein, we focus on how macrophages, immune cells well known for their tissue gatekeeping functions, assume fundamental, yet ill-defined, roles in the genesis and development of obesity-related metabolic disorders. We first discuss the determinants of the biology of these cells before introducing the specifics of the adipose tissue environment, while highlighting its heterogeneity. Finally, we detail how obesity transforms both adipose tissue and local macrophage populations. Understanding macrophage diversity and their cross talk with the diverse cell types constituting the adipose tissue environment will allow us to frame the therapeutic potential of adipose tissue macrophages in obesity.
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Affiliation(s)
- Svetoslav Chakarov
- Shanghai Institute of Immunology, Shanghai JiaoTong University School of Medicine, Shanghai, China
| | - Camille Blériot
- Institut Gustave Roussy, Batiment de Médecine Moléculaire, Villejuif, France
| | - Florent Ginhoux
- Shanghai Institute of Immunology, Shanghai JiaoTong University School of Medicine, Shanghai, China.,Institut Gustave Roussy, Batiment de Médecine Moléculaire, Villejuif, France.,Singapore Immunology Network, Agency for Science, Technology, and Research, Singapore, Singapore.,Translational Immunology Institute, SingHealth Duke-NUS Academic Medical Centre, Singapore, Singapore
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28
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Zhang X, Rotllan N, Canfrán-Duque A, Sun J, Toczek J, Moshnikova A, Malik S, Price NL, Araldi E, Zhong W, Sadeghi MM, Andreev OA, Bahal R, Reshetnyak YK, Suárez Y, Fernández-Hernando C. Targeted Suppression of miRNA-33 Using pHLIP Improves Atherosclerosis Regression. Circ Res 2022; 131:77-90. [PMID: 35534923 PMCID: PMC9640270 DOI: 10.1161/circresaha.121.320296] [Citation(s) in RCA: 42] [Impact Index Per Article: 14.0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Grants] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 10/06/2021] [Accepted: 05/03/2022] [Indexed: 11/16/2022]
Abstract
BACKGROUND miRNA therapeutics have gained attention during the past decade. These oligonucleotide treatments can modulate the expression of miRNAs in vivo and could be used to correct the imbalance of gene expression found in human diseases such as obesity, metabolic syndrome, and atherosclerosis. The in vivo efficacy of current anti-miRNA technologies hindered by physiological and cellular barriers to delivery into targeted cells and the nature of miRNAs that allows one to target an entire pathway that may lead to deleterious off-target effects. For these reasons, novel targeted delivery systems to inhibit miRNAs in specific tissues will be important for developing effective therapeutic strategies for numerous diseases including atherosclerosis. METHODS We used pH low-insertion peptide (pHLIP) constructs as vehicles to deliver microRNA-33-5p (miR-33) antisense oligonucleotides to atherosclerotic plaques. Immunohistochemistry and histology analysis was performed to assess the efficacy of miR-33 silencing in atherosclerotic lesions. We also assessed how miR-33 inhibition affects gene expression in monocytes/macrophages by single-cell RNA transcriptomics. RESULTS The anti-miR-33 conjugated pHLIP constructs are preferentially delivered to atherosclerotic plaque macrophages. The inhibition of miR-33 using pHLIP-directed macrophage targeting improves atherosclerosis regression by increasing collagen content and decreased lipid accumulation within vascular lesions. Single-cell RNA sequencing analysis revealed higher expression of fibrotic genes (Col2a1, Col3a1, Col1a2, Fn1, etc) and tissue inhibitor of metalloproteinase 3 (Timp3) and downregulation of Mmp12 in macrophages from atherosclerotic lesions targeted by pHLIP-anti-miR-33. CONCLUSIONS This study provides proof of principle for the application of pHLIP for treating advanced atherosclerosis via pharmacological inhibition of miR-33 in macrophages that avoid the deleterious effects in other metabolic tissues. This may open new therapeutic opportunities for atherosclerosis-associated cardiovascular diseases via selective delivery of other protective miRNAs.
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Affiliation(s)
- Xinbo Zhang
- Vascular Biology and Therapeutics Program, Yale University School of Medicine, New Haven, Connecticut, USA
- Integrative Cell Signaling and Neurobiology of Metabolism Program, Department of Comparative Medicine and Department of Pathology, Yale University School of Medicine, New Haven, Connecticut, USA
| | - Noemi Rotllan
- Vascular Biology and Therapeutics Program, Yale University School of Medicine, New Haven, Connecticut, USA
- Integrative Cell Signaling and Neurobiology of Metabolism Program, Department of Comparative Medicine and Department of Pathology, Yale University School of Medicine, New Haven, Connecticut, USA
| | - Alberto Canfrán-Duque
- Vascular Biology and Therapeutics Program, Yale University School of Medicine, New Haven, Connecticut, USA
- Integrative Cell Signaling and Neurobiology of Metabolism Program, Department of Comparative Medicine and Department of Pathology, Yale University School of Medicine, New Haven, Connecticut, USA
| | - Jonathan Sun
- Vascular Biology and Therapeutics Program, Yale University School of Medicine, New Haven, Connecticut, USA
- Integrative Cell Signaling and Neurobiology of Metabolism Program, Department of Comparative Medicine and Department of Pathology, Yale University School of Medicine, New Haven, Connecticut, USA
| | - Jakub Toczek
- Vascular Biology and Therapeutics Program, Yale University School of Medicine, New Haven, Connecticut, USA
- Cardiovascular Molecular Imaging Laboratory, Section of Cardiovascular Medicine and Yale Cardiovascular Research Center, Yale University School of Medicine, New Haven, Connecticut, USA
- Section of Cardiology, Veterans Affairs Connecticut Healthcare System, West Haven, CT, USA
| | - Anna Moshnikova
- Department Physics, University of Rhode Island, Kingston, Rhode Island, USA
| | - Shipra Malik
- Department of Pharmaceutical Sciences, University of Connecticut, Storrs, Connecticut, USA
| | - Nathan L. Price
- Vascular Biology and Therapeutics Program, Yale University School of Medicine, New Haven, Connecticut, USA
- Integrative Cell Signaling and Neurobiology of Metabolism Program, Department of Comparative Medicine and Department of Pathology, Yale University School of Medicine, New Haven, Connecticut, USA
| | - Elisa Araldi
- Vascular Biology and Therapeutics Program, Yale University School of Medicine, New Haven, Connecticut, USA
- Integrative Cell Signaling and Neurobiology of Metabolism Program, Department of Comparative Medicine and Department of Pathology, Yale University School of Medicine, New Haven, Connecticut, USA
| | - Wen Zhong
- Vascular Biology and Therapeutics Program, Yale University School of Medicine, New Haven, Connecticut, USA
- Integrative Cell Signaling and Neurobiology of Metabolism Program, Department of Comparative Medicine and Department of Pathology, Yale University School of Medicine, New Haven, Connecticut, USA
| | - Mehran M. Sadeghi
- Vascular Biology and Therapeutics Program, Yale University School of Medicine, New Haven, Connecticut, USA
- Cardiovascular Molecular Imaging Laboratory, Section of Cardiovascular Medicine and Yale Cardiovascular Research Center, Yale University School of Medicine, New Haven, Connecticut, USA
- Section of Cardiology, Veterans Affairs Connecticut Healthcare System, West Haven, CT, USA
| | - Oleg A. Andreev
- Department Physics, University of Rhode Island, Kingston, Rhode Island, USA
| | - Raman Bahal
- Department of Pharmaceutical Sciences, University of Connecticut, Storrs, Connecticut, USA
| | - Yana K. Reshetnyak
- Department Physics, University of Rhode Island, Kingston, Rhode Island, USA
| | - Yajaira Suárez
- Vascular Biology and Therapeutics Program, Yale University School of Medicine, New Haven, Connecticut, USA
- Integrative Cell Signaling and Neurobiology of Metabolism Program, Department of Comparative Medicine and Department of Pathology, Yale University School of Medicine, New Haven, Connecticut, USA
| | - Carlos Fernández-Hernando
- Vascular Biology and Therapeutics Program, Yale University School of Medicine, New Haven, Connecticut, USA
- Integrative Cell Signaling and Neurobiology of Metabolism Program, Department of Comparative Medicine and Department of Pathology, Yale University School of Medicine, New Haven, Connecticut, USA
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Liu L, Shi Z, Ji X, Zhang W, Luan J, Zahr T, Qiang L. Adipokines, adiposity, and atherosclerosis. Cell Mol Life Sci 2022; 79:272. [PMID: 35503385 PMCID: PMC11073100 DOI: 10.1007/s00018-022-04286-2] [Citation(s) in RCA: 69] [Impact Index Per Article: 23.0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Grants] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 01/10/2022] [Revised: 03/11/2022] [Accepted: 04/03/2022] [Indexed: 12/12/2022]
Abstract
Characterized by a surplus of whole-body adiposity, obesity is strongly associated with the prognosis of atherosclerosis, a hallmark of coronary artery disease (CAD) and the major contributor to cardiovascular disease (CVD) mortality. Adipose tissue serves a primary role as a lipid-storage organ, secreting cytokines known as adipokines that affect whole-body metabolism, inflammation, and endocrine functions. Emerging evidence suggests that adipokines can play important roles in atherosclerosis development, progression, as well as regression. Here, we review the versatile functions of various adipokines in atherosclerosis and divide these respective functions into three major groups: protective, deteriorative, and undefined. The protective adipokines represented here are adiponectin, fibroblast growth factor 21 (FGF-21), C1q tumor necrosis factor-related protein 9 (CTRP9), and progranulin, while the deteriorative adipokines listed include leptin, chemerin, resistin, Interleukin- 6 (IL-6), and more, with additional adipokines that have unclear roles denoted as undefined adipokines. Comprehensively categorizing adipokines in the context of atherosclerosis can help elucidate the various pathways involved and potentially pave novel therapeutic approaches to treat CVDs.
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Affiliation(s)
- Longhua Liu
- School of Kinesiology, Shanghai University of Sport, Shanghai, People's Republic of China.
| | - Zunhan Shi
- School of Kinesiology, Shanghai University of Sport, Shanghai, People's Republic of China
| | - Xiaohui Ji
- School of Kinesiology, Shanghai University of Sport, Shanghai, People's Republic of China
| | - Wenqian Zhang
- School of Kinesiology, Shanghai University of Sport, Shanghai, People's Republic of China
| | - Jinwen Luan
- School of Kinesiology, Shanghai University of Sport, Shanghai, People's Republic of China
| | - Tarik Zahr
- Department of Pharmacology, Columbia University, New York, NY, USA
| | - Li Qiang
- Department of Pathology and Cellular Biology and Naomi Berrie Diabetes Center, Columbia University, New York, NY, USA.
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Bielak K, Hołubowicz R, Zoglowek A, Żak A, Kędzierski P, Ożyhar A, Dobryszycki P. N'-terminal- and Ca 2+-induced stabilization of high-order oligomers of full-length Danio rerio and Homo sapiens otolin-1. Int J Biol Macromol 2022; 209:1032-1047. [PMID: 35447266 DOI: 10.1016/j.ijbiomac.2022.04.088] [Citation(s) in RCA: 1] [Impact Index Per Article: 0.3] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 03/04/2022] [Revised: 04/07/2022] [Accepted: 04/12/2022] [Indexed: 02/01/2023]
Abstract
Otolin-1 is a C1q family member and a major component of the organic matrix of fish otoliths and human otoconia. To date, the protein molecular properties have not been characterized. In this work, we describe biochemical characterization and comparative studies on saccular-specific otolin-1 derived from Danio rerio and Homo sapiens. Due to the low abundance of proteins in the otoconial matrix, we developed a production and purification method for both recombinant homologues of otolin-1. Danio rerio and Homo sapiens otolin-1 forms higher-order oligomers that can be partially disrupted under reducing conditions. The presence of Ca2+ stabilizes the oligomers and significantly increases the thermal stability of the proteins. Despite the high sequence coverage, the oligomerization of Danio rerio otolin-1 is more affected by the reducing conditions and presence of Ca2+ than the human homologue. The results show differences in molecular behaviour, which may be reflected in Danio rerio and Homo sapiens otolin-1 role in otolith and otoconia formation.
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Affiliation(s)
- Klaudia Bielak
- Department of Biochemistry, Molecular Biology and Biotechnology, Faculty of Chemistry, Wroclaw University of Science and Technology, Wroclaw, Poland
| | - Rafał Hołubowicz
- Department of Biochemistry, Molecular Biology and Biotechnology, Faculty of Chemistry, Wroclaw University of Science and Technology, Wroclaw, Poland
| | - Anna Zoglowek
- Department of Biochemistry, Molecular Biology and Biotechnology, Faculty of Chemistry, Wroclaw University of Science and Technology, Wroclaw, Poland
| | - Andrzej Żak
- Electron Microscopy Laboratory, Faculty of Mechanical Engineering, Wroclaw University of Science and Technology, Wroclaw, Poland
| | - Paweł Kędzierski
- Advanced Materials Engineering and Modelling Group, Faculty of Chemistry Wroclaw University of Science and Technology, Wroclaw, Poland
| | - Andrzej Ożyhar
- Department of Biochemistry, Molecular Biology and Biotechnology, Faculty of Chemistry, Wroclaw University of Science and Technology, Wroclaw, Poland
| | - Piotr Dobryszycki
- Department of Biochemistry, Molecular Biology and Biotechnology, Faculty of Chemistry, Wroclaw University of Science and Technology, Wroclaw, Poland.
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31
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Mahabadi AA, Anapliotis V, Dykun I, Hendricks S, Al-Rashid F, Lüdike P, Totzeck M, Rassaf T. Epicardial fat and incident heart failure with preserved ejection fraction in patients with coronary artery disease. Int J Cardiol 2022; 357:140-145. [PMID: 35395282 DOI: 10.1016/j.ijcard.2022.04.009] [Citation(s) in RCA: 6] [Impact Index Per Article: 2.0] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 11/02/2021] [Revised: 03/11/2022] [Accepted: 04/01/2022] [Indexed: 12/23/2022]
Abstract
BACKGROUND We aimed to determine, whether epicardial adipose tissue (EAT) as local source of inflammation, as well as its change over time, associates with the development of heart failure with preserved ejection fraction (HFpEF) in patients with coronary artery disease. METHODS AND RESULTS We retrospectively included 379patients (aged 65.2 ± 11.7 years, 70.2%male) with coronary artery disease but without heart failure at baseline, undergoing clinical and echocardiographic assessment in 2010-2013 and receiving a second assessment in 2014-2018. EAT thickness was defined as space between the myocardium and the pericardium and indexed (EATi) by body surface area. Change in EATi was calculated as the difference of follow-up and baseline EATi. HFpEF was defined according to presence of dyspnea, elevated natriuretic peptides, and structural and/or functional alterations on echocardiography in accordance with current European Society of Cardiology guidelines. During a median follow-up of 4.3 years, 142patients (37.5%) developed HFpEF. Patients with onset of HFpEF had higher EATi at baseline (2.4 ± 1.3 vs. 1.9 ± 0.9 mm/m2, p = 0.001). In multivariable regression analysis, EATi associated with onset of HFpEF (1.25 [1.01-1.54], p = 0.04). Likewise, an increase in EATi over time was linked HFpEF development, independent of other risk factors and baseline EATi (1.39 [1.04-1.87], p = 0.03). EATi was significantly associated with follow-up b-type natriuretic peptide (BNP) levels (4.31[0.58-8.05], p = 0.024), but not with baseline BNP (2.24[-0.27-4.76], p = 0.08). CONCLUSION EATi is associated with the development of HFpEF. The finding of changes in EATi altering the risk of HFpEF manifestation support the rationale for further research on epicardial fat modulation as a treatment target for HFpEF.
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Affiliation(s)
- Amir A Mahabadi
- West German Heart and Vascular Center Essen, Department of Cardiology and Vascular Medicine, University Hospital Essen, Hufelandstr. 55, 45147 Essen, Germany.
| | - Viktoria Anapliotis
- West German Heart and Vascular Center Essen, Department of Cardiology and Vascular Medicine, University Hospital Essen, Hufelandstr. 55, 45147 Essen, Germany
| | - Iryna Dykun
- Department of Cardiovascular Medicine, Heart, Vascular, and Thoracic Institute, Cleveland Clinic, Cleveland Clinic, Cleveland, OH, United States of America
| | - Stefanie Hendricks
- West German Heart and Vascular Center Essen, Department of Cardiology and Vascular Medicine, University Hospital Essen, Hufelandstr. 55, 45147 Essen, Germany
| | - Fadi Al-Rashid
- West German Heart and Vascular Center Essen, Department of Cardiology and Vascular Medicine, University Hospital Essen, Hufelandstr. 55, 45147 Essen, Germany
| | - Peter Lüdike
- West German Heart and Vascular Center Essen, Department of Cardiology and Vascular Medicine, University Hospital Essen, Hufelandstr. 55, 45147 Essen, Germany
| | - Matthias Totzeck
- West German Heart and Vascular Center Essen, Department of Cardiology and Vascular Medicine, University Hospital Essen, Hufelandstr. 55, 45147 Essen, Germany
| | - Tienush Rassaf
- West German Heart and Vascular Center Essen, Department of Cardiology and Vascular Medicine, University Hospital Essen, Hufelandstr. 55, 45147 Essen, Germany
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Jarrete AP, Giollo-Junior LT, Vilela-Martin JF, Novais IP, Delbin MA, Zanesco A. Alterations in pro- and anti-inflammatory mediators are involved in microvascular dysfunction in postmenopausal women with type 2 diabetes mellitus. Braz J Med Biol Res 2022; 55:e11821. [PMID: 35239779 PMCID: PMC8905673 DOI: 10.1590/1414-431x2021e11821] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 09/30/2021] [Accepted: 12/28/2021] [Indexed: 11/22/2022] Open
Abstract
Evidence has shown that women with type 2 diabetes mellitus (T2DM) have a greater
risk of cardiovascular complications compared with men, but this sex difference
is not clearly understood. This study assessed the microvascular function and
circulatory biomarkers in postmenopausal women (PMW) with T2DM compared with
diabetic men and their non-diabetic counterparts. Sixty participants were
divided into nondiabetic PMW, PMW with T2DM, non-diabetic men, and diabetic men.
Microvascular function was assessed using non-invasive equipment
(EndoPAT®) and reported as reactive hyperemia index (RHI).
Anthropometric and cardiovascular parameters were also measured. Two-way ANOVA
was performed using sex (women or men) and T2DM (non-diabetic and diabetic) as
the two factors. RHI impairment (1.97±0.14) was detected in diabetic PMW
compared with women without T2DM (2.5±0.13) accompanied by lower adiponectin
levels (T2DM: 9.3±1.2 and CTL: 13.8±1.8 ug/mL, P<0.05). An increase in the
Nε-carboxymethyllysine (CML), nitrate/nitrite, and C-reactive protein (CRP)
levels were observed in diabetic PMW compared to the other groups. Although a
poor glycemia control was seen in diabetic men, neither RHI nor circulatory
biomarkers were affected by T2DM. Multiple linear regression stratified by sex
and T2DM identified some variables with RHI only in PMW with T2DM: HbA1c
(P=0.003), body mass index (P=0.029), CML (P=0.032), and CRP (P=0.006). Diabetic
PMW were more susceptible to the deleterious effects of hyperglycemia than men,
showing microvascular dysfunction with high levels of pro-inflammatory mediators
(CML and CRP) and a lower adiponectin concentration.
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Affiliation(s)
- A P Jarrete
- Departamento de Biologia Estrutural e Funcional, Universidade Estadual de Campinas, Campinas, SP, Brasil
| | - L T Giollo-Junior
- Posto Médico Garrison - 5a Brigada de Cavalaria Blindada, Exército Brasileiro, Ponta Grossa, PR, Brasil
| | - J F Vilela-Martin
- Departamento de Medicina, Faculdade de Medicina de São José do Rio Preto, São José do Rio Preto, SP, Brasil
| | - I P Novais
- Departamento de Saúde I, Universidade Estadual do Sudoeste da Bahia, Jequié, BA, Brasil
| | - M A Delbin
- Departamento de Biologia Estrutural e Funcional, Universidade Estadual de Campinas, Campinas, SP, Brasil
| | - A Zanesco
- Programa de Pós-Graduação em Saúde e Meio-ambiente, Faculdade de Medicina, Universidade Metropolitana de Santos, Santos, SP, Brasil
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Wang YY, Wang YD, Qi XY, Liao ZZ, Mai YN, Xiao XH. Organokines and Exosomes: Integrators of Adipose Tissue Macrophage Polarization and Recruitment in Obesity. Front Endocrinol (Lausanne) 2022; 13:839849. [PMID: 35273574 PMCID: PMC8902818 DOI: 10.3389/fendo.2022.839849] [Citation(s) in RCA: 13] [Impact Index Per Article: 4.3] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 12/20/2021] [Accepted: 01/24/2022] [Indexed: 12/21/2022] Open
Abstract
The prevalence of obesity is escalating and has become a worldwide health challenge coinciding with the development of metabolic diseases. Emerging evidence has shown that obesity is accompanied by the infiltration of macrophages into adipose tissue, contributing to a state of low-grade chronic inflammation and dysregulated metabolism. Moreover, in the state of obesity, the phenotype of adipose tissue macrophages switches from the M2 polarized state to the M1 state, thereby contributing to chronic inflammation. Notably, multiple metabolic organs (adipose tissue, gut, skeletal muscle, and the liver) communicate with adipose tissue macrophages via secreting organokines or exosomes. In this review, we systematically summarize how the organokines (adipokines, gut microbiota and its metabolites, gut cytokines, myokines, and hepatokines) and exosomes (adipocyte-, skeletal muscle-, and hepatocyte-derived exosomes) act as important triggers for macrophage recruitment in adipose tissue and adipose tissue macrophage polarization, thus providing further insight into obesity treatment. In addition, we also highlight the complex interaction of organokines with organokines and organokines with exosomes, revealing new paths in understanding adipose tissue macrophage recruitment and polarization.
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Affiliation(s)
| | | | | | | | | | - Xin-Hua Xiao
- The First Affiliated Hospital, Department of Metabolism and Endocrinology, Hengyang Medical School, University of South China, Hengyang, China
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Yurtcu N, Caliskan CS, Guvey H, Celik S, Hatirnaz S, Tinelli A. Predictive and Diagnostic Value of Serum Adipokines in Pregnant Women with Intrahepatic Cholestasis. INTERNATIONAL JOURNAL OF ENVIRONMENTAL RESEARCH AND PUBLIC HEALTH 2022; 19:ijerph19042254. [PMID: 35206438 PMCID: PMC8871533 DOI: 10.3390/ijerph19042254] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Download PDF] [Figures] [Subscribe] [Scholar Register] [Received: 11/28/2021] [Revised: 02/07/2022] [Accepted: 02/09/2022] [Indexed: 11/16/2022]
Abstract
The objective of this study was to assess the value of serum leptin, adiponectin, apelin, and ghrelin as biomarkers for the prediction and diagnosis of intra-hepatic cholestasis (ICP). This prospective study included pregnant women in the third trimester of pregnancy: 63 with ICP, 48 and 15 of whom had mild and severe disease, respectively, and 32 as controls. ICP women had increased median levels of serum leptin, adiponectin, apelin, and ghrelin compared to the controls (p < 0.05). These biomarkers meaningfully changed regarding the severity of ICP: While leptin was reduced, apelin and ghrelin were increased, and adiponectin was increased somewhat. To predict and diagnose ICP, the predictive values of serum leptin, adiponectin, and apelin need to be accepted as comparable, with moderate to high sensitivity and specificity; however, the predictive value of serum ghrelin was somewhat lower. More research is needed to clarify the potential properties of adipokines to gain acceptance as a predictive or diagnostic biomarker for ICP.
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Affiliation(s)
- Nazan Yurtcu
- Department of Obstetrics and Gynecology, Sivas Cumhuriyet University Faculty of Medicine, Sivas 58140, Turkey
- Correspondence:
| | - Canan Soyer Caliskan
- Department of Obstetrics and Gynecology, Samsun Training and Research Hospital, Health Sciences University, Samsun 55270, Turkey; (C.S.C.); (S.C.)
| | - Huri Guvey
- Department of Obstetrics and Gynecology, Private Kütahya Parkhayat Hospital, Kütahya 43100, Turkey;
| | - Samettin Celik
- Department of Obstetrics and Gynecology, Samsun Training and Research Hospital, Health Sciences University, Samsun 55270, Turkey; (C.S.C.); (S.C.)
| | - Safak Hatirnaz
- In Vitro Fertilization Unit, Medicana International Hospital, Samsun 55080, Turkey;
| | - Andrea Tinelli
- Department of Obstetrics and Gynecology, Veris delli Ponti Hospital, 73020 Lecce, Italy;
- Department of Obstetrics and Gynecology, Division of Experimental Endoscopic Surgery, Imaging, Technology and Minimally Invasive Therapy, Vito Fazzi Hospital, 73100 Lecce, Italy
- Phystech BioMed School, Faculty of Biological & Medical Physics, Moscow Institute of Physics and Technology, State University, 141701 Moscow, Russia
- Xi’an Jiaotong University, Xi’an 710049, China
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Zambon Azevedo V, Silaghi CA, Maurel T, Silaghi H, Ratziu V, Pais R. Impact of Sarcopenia on the Severity of the Liver Damage in Patients With Non-alcoholic Fatty Liver Disease. Front Nutr 2022; 8:774030. [PMID: 35111794 PMCID: PMC8802760 DOI: 10.3389/fnut.2021.774030] [Citation(s) in RCA: 24] [Impact Index Per Article: 8.0] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 09/10/2021] [Accepted: 12/21/2021] [Indexed: 12/12/2022] Open
Abstract
An extensive body of the literature shows a strong interrelationship between the pathogenic pathways of non-alcoholic fatty liver disease (NAFLD) and sarcopenia through the muscle-liver-adipose tissue axis. NAFLD is one of the leading causes of chronic liver diseases (CLD) affecting more than one-quarter of the general population worldwide. The disease severity spectrum ranges from simple steatosis to non-alcoholic steatohepatitis (NASH), cirrhosis, and its complications: end-stage chronic liver disease and hepatocellular carcinoma. Sarcopenia, defined as a progressive loss of the skeletal muscle mass, reduces physical performances, is associated with metabolic dysfunction and, possibly, has a causative role in NAFLD pathogenesis. Muscle mass is a key determinant of the whole-body insulin-mediated glucose metabolism and impacts fatty liver oxidation and energy homeostasis. These mechanisms drive the accumulation of ectopic fat both in the liver (steatosis, fatty liver) and in the muscle (myosteatosis). Myosteatosis rather than the muscle mass per se, seems to be closely associated with the severity of the liver injury. Sarcopenic obesity is a recently described entity which associates both sarcopenia and obesity and may trigger worse clinical outcomes including hepatic fibrosis progression and musculoskeletal disabilities. Furthermore, the muscle-liver-adipose tissue axis has a pivotal role in changes of the body composition, resulting in a distinct clinical phenotype that enables the identification of the "sarcopenic NAFLD phenotype." This review aims to bring some light into the complex relationship between sarcopenia and NAFLD and critically discuss the key mechanisms linking NAFLD to sarcopenia, as well as some of the clinical consequences associated with the coexistence of these two entities: the impact of body composition phenotypes on muscle morphology, the concept of sarcopenic obesity, the relationship between sarcopenia and the severity of the liver damage and finally, the future directions and the existing gaps in the knowledge.
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Affiliation(s)
- Vittoria Zambon Azevedo
- Doctoral School Physiology, Physiopathology and Therapeutics 394, Sorbonne Université, Paris, France
- Centre de Recherche de Cordeliers, INSERM UMRS 1138, Paris, France
| | - Cristina Alina Silaghi
- Department of Endocrinology, “Iuliu Hatieganu” University of Medicine and Pharmacy Cluj-Napoca, Cluj-Napoca, Romania
| | - Thomas Maurel
- Institute of Cardiometabolism and Nutrition, Paris, France
- Assistance Publique Hôpitaux de Paris, Hôpital Pitié-Salpêtrière, Paris, France
| | - Horatiu Silaghi
- Department of Surgery V, “Iuliu Hatieganu” University of Medicine and Pharmacy Cluj-Napoca, Cluj-Napoca, Romania
| | - Vlad Ratziu
- Centre de Recherche de Cordeliers, INSERM UMRS 1138, Paris, France
- Institute of Cardiometabolism and Nutrition, Paris, France
- Assistance Publique Hôpitaux de Paris, Hôpital Pitié-Salpêtrière, Paris, France
- Sorbonne Université, Paris, France
| | - Raluca Pais
- Institute of Cardiometabolism and Nutrition, Paris, France
- Assistance Publique Hôpitaux de Paris, Hôpital Pitié-Salpêtrière, Paris, France
- Sorbonne Université, Paris, France
- Centre de Recherche Saint Antoine, INSERM UMRS 938, Paris, France
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Metabolic Syndrome: Updates on Pathophysiology and Management in 2021. Int J Mol Sci 2022; 23:ijms23020786. [PMID: 35054972 PMCID: PMC8775991 DOI: 10.3390/ijms23020786] [Citation(s) in RCA: 625] [Impact Index Per Article: 208.3] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 11/17/2021] [Revised: 12/22/2021] [Accepted: 12/23/2021] [Indexed: 12/18/2022] Open
Abstract
Metabolic syndrome (MetS) forms a cluster of metabolic dysregulations including insulin resistance, atherogenic dyslipidemia, central obesity, and hypertension. The pathogenesis of MetS encompasses multiple genetic and acquired entities that fall under the umbrella of insulin resistance and chronic low-grade inflammation. If left untreated, MetS is significantly associated with an increased risk of developing diabetes and cardiovascular diseases (CVDs). Given that CVDs constitute by far the leading cause of morbidity and mortality worldwide, it has become essential to investigate the role played by MetS in this context to reduce the heavy burden of the disease. As such, and while MetS relatively constitutes a novel clinical entity, the extent of research about the disease has been exponentially growing in the past few decades. However, many aspects of this clinical entity are still not completely understood, and many questions remain unanswered to date. In this review, we provide a historical background and highlight the epidemiology of MetS. We also discuss the current and latest knowledge about the histopathology and pathophysiology of the disease. Finally, we summarize the most recent updates about the management and the prevention of this clinical syndrome.
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The Effect of Herbal Medicine and Natural Bioactive Compounds on Plasma Adiponectin: A Clinical Review. ADVANCES IN EXPERIMENTAL MEDICINE AND BIOLOGY 2022; 1328:37-57. [PMID: 34981470 DOI: 10.1007/978-3-030-73234-9_4] [Citation(s) in RCA: 1] [Impact Index Per Article: 0.3] [Reference Citation Analysis] [Abstract] [Key Words] [Subscribe] [Scholar Register] [Indexed: 12/12/2022]
Abstract
Noncommunicable diseases (NCDs) are one of the major public health concerns globally. Most of the NCDs including insulin resistance, metabolic syndrome, type 2 diabetes mellitus, fatty liver disease, and coronary heart disease are related to obesity and are called obesity-related NCDs (OR-NCDs). However, adipocytes can reduce OR-NCDs by secreting adiponectin. Adiponectin has an inverse relationship with body fat. Obese people have impairment in differentiating pre-adipocytes to adipocytes, the process facilitated by adiponectin. Adiponectin directly increases insulin sensitivity and reduces obesity-related insulin resistance by down-regulating hepatic glucose production and increasing fatty acid (FA) oxidation in skeletal muscle. Considering the various beneficial effects of adiponectin on health, increasing adiponectin might be a promising approach to prevent and treat OR-NCDs. Recent studies have shown that nutraceuticals and medicinal compounds isolated from plants could prevent and treat various diseases, particularly cardiovascular diseases (CVDs), diabetes mellitus, obesity, and non-alcoholic fatty liver disease. However, to our knowledge, the effect of these natural products, including herbal supplements and functional foods on adiponectin, has not yet been fully reviewed. The main aim of this review is to summarize the effects of nutraceuticals and herbal bioactive compounds on plasma adiponectin concentrations based on clinical studies. It can be concluded that medicinal plants, and herbal bioactive compounds, particularly curcumin, anthocyanins, resveratrol, soy, walnut, and dihydromyricetin can be used as adjunct or complementary therapeutic agents to increase plasma adiponectin, which could potentially prevent and treat NCDs.
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The Roles and Associated Mechanisms of Adipokines in Development of Metabolic Syndrome. MOLECULES (BASEL, SWITZERLAND) 2022; 27:molecules27020334. [PMID: 35056647 PMCID: PMC8781412 DOI: 10.3390/molecules27020334] [Citation(s) in RCA: 72] [Impact Index Per Article: 24.0] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Figures] [Subscribe] [Scholar Register] [Received: 11/09/2021] [Revised: 12/30/2021] [Accepted: 01/03/2022] [Indexed: 12/12/2022]
Abstract
Metabolic syndrome is a cluster of metabolic indicators that increase the risk of diabetes and cardiovascular diseases. Visceral obesity and factors derived from altered adipose tissue, adipokines, play critical roles in the development of metabolic syndrome. Although the adipokines leptin and adiponectin improve insulin sensitivity, others contribute to the development of glucose intolerance, including visfatin, fetuin-A, resistin, and plasminogen activator inhibitor-1 (PAI-1). Leptin and adiponectin increase fatty acid oxidation, prevent foam cell formation, and improve lipid metabolism, while visfatin, fetuin-A, PAI-1, and resistin have pro-atherogenic properties. In this review, we briefly summarize the role of various adipokines in the development of metabolic syndrome, focusing on glucose homeostasis and lipid metabolism.
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39
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Tyagi N, Kaur C. Role of serum adiponectin levels and IL-10 as a marker for angiographic stenosis in coronary artery disease. INTERNATIONAL JOURNAL OF THE CARDIOVASCULAR ACADEMY 2022. [DOI: 10.4103/ijca.ijca_47_21] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 11/04/2022] Open
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40
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Tanyanskiy DA, Pigarevskii PV, Maltseva SV, Malashicheva AB, Docshin PM, Uspenskiy VE, Lizunov AV, Orlov SV, Maltseva ON, Ageeva EV, Denisenko AD. [Adiponectin in normal and atherosclerotic intima of human aorta]. Arkh Patol 2022; 84:16-22. [PMID: 36469713 DOI: 10.17116/patol20228406116] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 06/17/2023]
Abstract
BACKGROUND Adiponectin (AN) is a protein synthesized by adipocytes that has regulatory effects on lipid and lipoprotein metabolism, increases tissue sensitivity to insulin, and modulates endothelial functions and inflammatory response. However, its involvement in the processes of atherogenesis remains poorly understood. OBJECTIVE To determine the localization and sources of AN in atherosclerotic and normal human aortic intima. MATERIAL AND METHODS Immunohistochemical study was performed on sections of atherosclerotic and normal human aorta obtained during autopsy. Reverse transcription real-time PCR was performed using biopsies of para-aortic and abdominal adipose tissue, intima-media of the thoracic aorta, atherosclerotic plaques of the human carotid and femoral arteries, as well as on endothelial cells isolated from the human thoracic aorta. Transendothelial transport of AN was evaluated in a two-chamber model using a monolayer of human endothelial cell hybridoma EA.Hy926. RESULTS It has been established that AN is present in atherosclerotic but not in normal human aortic intima. At the same time, AN ADIPOQ mRNA was not detected either in the intima media of the human aorta, nor in isolated endothelial cells of the aorta, nor in cells of atherosclerotic plaques of the carotid and femoral arteries. AN slowly penetrated the endothelial monolayer in vitro, but this transport was significantly enhanced by the action of tumor necrosis factor-alpha (TNFa). CONCLUSION Obtained data indicate that AN is present in atherosclerotic but not in normal aortic intima. We assume that AN is not synthesized by the cells of normal and atherosclerotic arterial walls, but permeates from the plasma. Transendothelial transport of AN, like many other plasma proteins, is activated during the development of atherosclerotic lesions, apparently under the action of pro-inflammatory cytokines, in particular, TNFα.
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Affiliation(s)
- D A Tanyanskiy
- Institute of Experimental Medicine, St. Petersburg, Russia
- Saint Petersburg State University, St. Petersburg, Russia
| | | | - S V Maltseva
- Institute of Experimental Medicine, St. Petersburg, Russia
| | - A B Malashicheva
- Institute of Cytology Russian Academy of Science, St. Petersburg, Russia
| | - P M Docshin
- Almazov National Medical Research Centre, St. Petersburg, Russia
| | - V E Uspenskiy
- Almazov National Medical Research Centre, St. Petersburg, Russia
| | - A V Lizunov
- Institute of Experimental Medicine, St. Petersburg, Russia
- Saint Petersburg State University, St. Petersburg, Russia
| | - S V Orlov
- Institute of Experimental Medicine, St. Petersburg, Russia
- Saint Petersburg State University, St. Petersburg, Russia
| | - O N Maltseva
- Institute of Experimental Medicine, St. Petersburg, Russia
| | - E V Ageeva
- Institute of Experimental Medicine, St. Petersburg, Russia
| | - A D Denisenko
- Institute of Experimental Medicine, St. Petersburg, Russia
- Saint Petersburg State University, St. Petersburg, Russia
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Marjani M, Dolab N, Kamkar MZ, Amiriani T, Yuzugulen J, Marjani A. Gender and Body Mass Index-Related Serum Level of Adipokines and Metabolic Syndrome Components in Bipolar Patients who received Lithium and Valproic Acid. Metab Syndr Relat Disord 2021; 20:79-87. [PMID: 34874780 DOI: 10.1089/met.2021.0078] [Citation(s) in RCA: 3] [Impact Index Per Article: 0.8] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 12/26/2022] Open
Abstract
Background: This is the study to assess alterations on adiponectin, leptin, and metabolic syndrome components in women and men bipolar disorder (BD) patients with normal weight and obesity who received valproic acid (VPA) and lithium (Li). Methods: Thirty-six women and 51 men were included. Commercial kits were used to determine all parameters. Metabolic syndrome components were determined according to the NCEP ATP III criteria. Results: Patients who received Li and VPA significantly differ in waist circumference (WC) and triglyceride (TG) levels (in women and men). Normal weight patients received both drugs, significant differences were considered in high-density lipoprotein-cholesterol (HDL-C), WC, and TG levels compared to healthy controls, but there were significant differences in TG, leptin, and adiponectin levels in obese patients who received VPA. There were significant negative and positive correlation between leptin and adiponectin and WC and TG in women and men BD patients treated with VPA and Li. There were significant positive correlation between leptin and adiponectin and WC and TG and significant negative correlation with HDL-C in normal weight BD patients treated with VPA and Li, respectively, while there was only a significant positive correlation between leptin and adiponectin, and TG in obese BD patients treated with VPA. Conclusions: It looks like that patients treated with both drugs for our suggested time may increase leptin and adiponectin levels. Correlation differences between leptin and adiponectin, and metabolic syndrome components may be important parameters in women, men, normal weight, and obese BD patients. Monitoring of body composition and adipokines may benefit in medical care of these patients.
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Affiliation(s)
- Majid Marjani
- Faculty of Pharmacy, Eastern Mediterranean University, Famagusta, Turkey
| | - Neda Dolab
- Student Research Committee, Department of Biochemistry and Biophysics, Gorgan Faculty of Medicine, Metabolic Disorders Research Center, Golestan University Medical Sciences, Gorgan, Iran
| | - Mohammad Zaman Kamkar
- Department of Psychiatry, Golestan Research Center of Psychiatry, Golestan University of Medical Sciences, Gorgan, Iran
| | - Taghi Amiriani
- Golestan Research Center of Gastroenterology and Hepatology, Golestan University of Medical Sciences, Gorgan, Iran
| | - Jale Yuzugulen
- Faculty of Pharmacy, Eastern Mediterranean University, Famagusta, Turkey
| | - Abdoljalal Marjani
- Department of Biochemistry and Biophysics, Faculty of Medicine, Metabolic Disorders Research Center, Golestan University of Medical Sciences, Gorgan, Iran
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Zou X, Wang L, Xiao L, Xu Z, Yao T, Shen M, Zeng Y, Zhang L. Deciphering the Irregular Risk of Stroke Increased by Obesity Classes: A Stratified Mendelian Randomization Study. Front Endocrinol (Lausanne) 2021; 12:750999. [PMID: 34925231 PMCID: PMC8671740 DOI: 10.3389/fendo.2021.750999] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 07/31/2021] [Accepted: 11/08/2021] [Indexed: 11/13/2022] Open
Abstract
BACKGROUND To investigate the relationship between different classes of obesity and stroke, we conducted a stratified Mendelian randomization (MR) study. METHODS The body mass index (BMI) data of 263,407 Europeans with three classes of obesity (obesity class I, 30 kg/m2 ≤ BMI < 35 kg/m2; obesity class II, 35 kg/m2 ≤ BMI < 40 kg/m2; obesity class III, 40 kg/m2 ≤ BMI) were extracted from the Genetic Investigation of ANthropometric Traits (GIANT) consortium. Summary-level data of stroke and its subtypes [ischemic stroke (IS) and intracerebral hemorrhage (ICH)] were obtained from the genome-wide association study (GWAS) meta-analysis, which was performed by the MEGASTROKE consortium. MR methods were used to identify the causal relationships. RESULTS The MR analysis revealed that both obesity class I [odds ratio (OR) = 1.08, 95% CI: 1.05-1.12, p = 1.0 × 10-5] and obesity class II (OR = 1.06, 95% CI: 1.03-1.09, p = 1 × 10-4) were significantly positively related to IS, while obesity class III was not (OR = 1.01, 95% CI: 0.96-1.06, p = 0.65). In contrast to IS, there was no class of obesity associated with ICH risk. Further examination of the relationship between obesity classification and IS subtypes revealed that certain degrees of obesity were related to large artery stroke (LAS) (OR = 1.14, 95% CI: 1.04-1.24, p = 2.8 × 10-3 for class I; OR = 1.08, 95% CI: 1.01-1.16, p = 0.002 for class II) and cardioembolic stroke (CES) (OR = 1.11, 95% CI: 1.02-1.20, p = 0.02 for class I; OR = 1.08, 95% CI: 1.02-1.15, p = 0.007 for class II). CONCLUSIONS A higher risk of IS, but not ICH, could be linked to obesity classes I and II. A strong association between LAS and CES and obesity was observed among all IS subtypes in the obese population.
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Affiliation(s)
- Xuelun Zou
- Department of Neurology, Xiangya Hospital, Central South University, Changsha, China
| | - Leiyun Wang
- Department of Clinical Pharmacology, Xiangya Hospital, Central South University, Changsha, China
- Institute of Clinical Pharmacology, Central South University, Hunan Key Laboratory of Pharmacogenetics, Changsha, China
| | - Linxiao Xiao
- Department of Spine Surgery and Orthopaedics, Xiangya Hospital, Central South University, Changsha, China
| | - Zihao Xu
- Department of Neurology, Xiangya Hospital, Central South University, Changsha, China
| | - Tianxing Yao
- Department of Neurology, Xiangya Hospital, Central South University, Changsha, China
| | - Minxue Shen
- Department of Epidemiology and Health Statistics, Xiangya School of Public Health, Central South University, Changsha, China
| | - Yi Zeng
- Department of Geriatrics, Second Xiangya Hospital, Central South University, Changsha, China
| | - Le Zhang
- Department of Neurology, Xiangya Hospital, Central South University, Changsha, China
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C1q tumor necrosis factor-related protein 1: a promising therapeutic target for atherosclerosis. J Cardiovasc Pharmacol 2021; 79:273-280. [PMID: 34840267 DOI: 10.1097/fjc.0000000000001186] [Citation(s) in RCA: 3] [Impact Index Per Article: 0.8] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 09/15/2021] [Accepted: 11/06/2021] [Indexed: 11/25/2022]
Abstract
ABSTRACT Atherosclerosis serves as the pathological basis of most cardiovascular and cerebrovascular diseases. C1q tumor necrosis factor-related protein (CTRP1) is a 35-kDa glycoprotein synthesized by various tissues and cells, such as adipose tissue and macrophages. As an adiponectin paralog, CTRP1 signals through adiponectin receptor 1 (AdipoR1) and participates in a variety of pathophysiological processes. Circulating CTRP1 levels are significantly increased in patients with coronary artery disease. Importantly, CTRP1 was shown to accelerate the development of atherosclerosis by promoting vascular inflammation, macrophage foam cell formation and endothelial barrier dysfunction. This review focused on recent advances regarding the role of CTRP1 in atherogenesis with an emphasis on its potential as a novel biomarker and a promising therapeutic target for atherosclerosis-related diseases.
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Age and Sex: Impact on adipose tissue metabolism and inflammation. Mech Ageing Dev 2021; 199:111563. [PMID: 34474078 DOI: 10.1016/j.mad.2021.111563] [Citation(s) in RCA: 38] [Impact Index Per Article: 9.5] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 03/26/2021] [Revised: 08/19/2021] [Accepted: 08/26/2021] [Indexed: 02/08/2023]
Abstract
Age associated chronic inflammation is a major contributor to diseases with advancing age. Adipose tissue function is at the nexus of processes contributing to age-related metabolic disease and mediating longevity. Hormonal fluctuations in aging potentially regulate age-associated visceral adiposity and metabolic dysfunction. Visceral adiposity in aging is linked to aberrant adipogenesis, insulin resistance, lipotoxicity and altered adipokine secretion. Age-related inflammatory phenomena depict sex differences in macrophage polarization, changes in T and B cell numbers, and types of dendritic cells. Sex differences are also observed in adipose tissue remodeling and cellular senescence suggesting a role for sex steroid hormones in the regulation of the adipose tissue microenvironment. It is crucial to investigate sex differences in aging clinical outcomes to identify and better understand physiology in at-risk individuals. Early interventions aimed at targets involved in adipose tissue adipogenesis, remodeling and inflammation in aging could facilitate a profound impact on health span and overcome age-related functional decline.
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Tanyanskiy DA, Trulioff AS, Ageeva EV, Nikitin AA, Shavva VS, Orlov SV. The Influence of Adiponectin on Production of Apolipoproteins A-1 and E by Human Macrophages. Mol Biol 2021. [DOI: 10.1134/s0026893321030122] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 11/23/2022]
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Zhou X, Shafique K, Sajid M, Ali Q, Khalili E, Javed MA, Haider MS, Zhou G, Zhu G. Era-like GTP protein gene expression in rice. BRAZ J BIOL 2021; 82:e250700. [PMID: 34259718 DOI: 10.1590/1519-6984.250700] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Journal Information] [Subscribe] [Scholar Register] [Received: 04/05/2021] [Accepted: 06/19/2021] [Indexed: 11/22/2022] Open
Abstract
The mutations are genetic changes in the genome sequences and have a significant role in biotechnology, genetics, and molecular biology even to find out the genome sequences of a cell DNA along with the viral RNA sequencing. The mutations are the alterations in DNA that may be natural or spontaneous and induced due to biochemical reactions or radiations which damage cell DNA. There is another cause of mutations which is known as transposons or jumping genes which can change their position in the genome during meiosis or DNA replication. The transposable elements can induce by self in the genome due to cellular and molecular mechanisms including hypermutation which caused the localization of transposable elements to move within the genome. The use of induced mutations for studying the mutagenesis in crop plants is very common as well as a promising method for screening crop plants with new and enhanced traits for the improvement of yield and production. The utilization of insertional mutations through transposons or jumping genes usually generates stable mutant alleles which are mostly tagged for the presence or absence of jumping genes or transposable elements. The transposable elements may be used for the identification of mutated genes in crop plants and even for the stable insertion of transposable elements in mutated crop plants. The guanine nucleotide-binding (GTP) proteins have an important role in inducing tolerance in rice plants to combat abiotic stress conditions.
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Affiliation(s)
- X Zhou
- Linyi University, College of Life Science, Linyi, Shandong, China
| | - K Shafique
- Government Sadiq College Women University, Department of Botany, Bahawalpur, Pakistan
| | - M Sajid
- University of Okara, Faculty of Life Sciences, Department of Biotechnology, Okara, Pakistan
| | - Q Ali
- University of Lahore, Institute of Molecular Biology and Biotechnology, Lahore, Pakistan
| | - E Khalili
- Tarbiat Modarres University, Faculty of Science, Department of Plant Science, Tehran, Iran
| | - M A Javed
- University of the Punjab Lahore, Department of Plant Breeding and Genetics, Lahore, Pakistan
| | - M S Haider
- University of the Punjab Lahore, Department of Plant Pathology, Lahore, Pakistan
| | - G Zhou
- Yangzhou University, The Ministry of Education of China, Joint International Research Laboratory of Agriculture and Agri-Product Safety, Yangzhou, Jiangsu, China
| | - G Zhu
- Yangzhou University, The Ministry of Education of China, Joint International Research Laboratory of Agriculture and Agri-Product Safety, Yangzhou, Jiangsu, China
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Sowka A, Dobrzyn P. Role of Perivascular Adipose Tissue-Derived Adiponectin in Vascular Homeostasis. Cells 2021; 10:cells10061485. [PMID: 34204799 PMCID: PMC8231548 DOI: 10.3390/cells10061485] [Citation(s) in RCA: 35] [Impact Index Per Article: 8.8] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 05/11/2021] [Revised: 06/04/2021] [Accepted: 06/08/2021] [Indexed: 12/27/2022] Open
Abstract
Studies of adipose tissue biology have demonstrated that adipose tissue should be considered as both passive, energy-storing tissue and an endocrine organ because of the secretion of adipose-specific factors, called adipokines. Adiponectin is a well-described homeostatic adipokine with metabolic properties. It regulates whole-body energy status through the induction of fatty acid oxidation and glucose uptake. Adiponectin also has anti-inflammatory and antidiabetic properties, making it an interesting subject of biomedical studies. Perivascular adipose tissue (PVAT) is a fat depot that is conterminous to the vascular wall and acts on it in a paracrine manner through adipokine secretion. PVAT-derived adiponectin can act on the vascular wall through endothelial cells and vascular smooth muscle cells. The present review describes adiponectin's structure, receptors, and main signaling pathways. We further discuss recent studies of the extent and nature of crosstalk between PVAT-derived adiponectin and endothelial cells, vascular smooth muscle cells, and atherosclerotic plaques. Furthermore, we argue whether adiponectin and its receptors may be considered putative therapeutic targets.
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12-Hydroxyeicosapentaenoic acid inhibits foam cell formation and ameliorates high-fat diet-induced pathology of atherosclerosis in mice. Sci Rep 2021; 11:10426. [PMID: 34001916 PMCID: PMC8129127 DOI: 10.1038/s41598-021-89707-1] [Citation(s) in RCA: 21] [Impact Index Per Article: 5.3] [Reference Citation Analysis] [Abstract] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 12/28/2020] [Accepted: 04/26/2021] [Indexed: 02/02/2023] Open
Abstract
Atherosclerosis is a chronic inflammatory disease associated with macrophage aggregate and transformation into foam cells. In this study, we sought to investigate the impact of dietary intake of ω3 fatty acid on the development of atherosclerosis, and demonstrate the mechanism of action by identifying anti-inflammatory lipid metabolite. Mice were exposed to a high-fat diet (HFD) supplemented with either conventional soybean oil or α-linolenic acid-rich linseed oil. We found that as mice became obese they also showed increased pulsatility and resistive indexes in the common carotid artery. In sharp contrast, the addition of linseed oil to the HFD improved pulsatility and resistive indexes without affecting weight gain. Histological analysis revealed that dietary linseed oil inhibited foam cell formation in the aortic valve. Lipidomic analysis demonstrated a particularly marked increase in the eicosapentaenoic acid-derived metabolite 12-hydroxyeicosapentaenoic acid (12-HEPE) in the serum from mice fed with linseed oil. When we gave 12-HEPE to mice with HFD, the pulsatility and resistive indexes was improved. Indeed, 12-HEPE inhibited the foamy transformation of macrophages in a peroxisome proliferator-activated receptor (PPAR)γ-dependent manner. These results demonstrate that the 12-HEPE-PPARγ axis ameliorates the pathogenesis of atherosclerosis by inhibiting foam cell formation.
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Preterm human milk: associations between perinatal factors and hormone concentrations throughout lactation. Pediatr Res 2021; 89:1461-1469. [PMID: 32726796 DOI: 10.1038/s41390-020-1069-1] [Citation(s) in RCA: 11] [Impact Index Per Article: 2.8] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 04/15/2020] [Revised: 07/08/2020] [Accepted: 07/12/2020] [Indexed: 12/14/2022]
Abstract
BACKGROUND Infants born moderate to late preterm constitute the majority of preterm births, yet guidelines for their nutritional care are unclear. Maternal milk is the most appropriate nutrition for these infants; however, its composition can be influenced by environmental factors. The present study therefore investigated perinatal predictors of human milk composition in a preterm cohort. METHODS Milk was collected during the DIAMOND trial (DIfferent Approaches to Moderate and late preterm Nutrition: Determinants of feed tolerance, body composition and development) from 169 mothers of 191 infants at three time-points (5 and 10 days post partum and 4 months' corrected age). Leptin, adiponectin and insulin-like growth factor-1 (IGF-1) were analysed by enzyme-linked immunosorbent assay. Generalised mixed models were used to evaluate associations between milk composition and maternal/infant/perinatal factors. RESULTS Most findings were independent of collection time-point. Gestational diabetes was associated with lower adiponectin. Higher adiponectin and lower leptin were associated with higher socioeconomic status, higher maternal education and ability to fully breastfeed at discharge from hospital. Higher leptin was associated with high perceived stress during hospital admission. Milk IGF-1 displayed sex-specific patterns in association with maternal social deprivation. CONCLUSION Maternal, infant and environmental factors during the perinatal period were associated with milk compositional profiles throughout lactation. Further clinical trials should investigate the impact of such changes in terms of long-term infant outcomes. IMPACT Human milk is the best nutrition for the infant. However, its composition may be susceptible to alterations determined by pathological conditions mother and infant may face throughout pregnancy and in the perinatal period. This study found that perinatal factors are associated with human milk composition from early to late lactation. If human milk composition throughout lactation is "programmed" during pregnancy or early lactation, infants who were exposed in utero to environmental insults may still be exposed to them during lactation. The impact of human milk compositional alteration on infant growth following perinatal pathological events requires further investigation.
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Shan D, Dou G, Yang J, Wang X, Wang J, Zhang W, He B, Liu Y, Chen Y, Li Y. Epicardial Adipose Tissue Volume Is Associated with High Risk Plaque Profiles in Suspect CAD Patients. OXIDATIVE MEDICINE AND CELLULAR LONGEVITY 2021; 2021:6663948. [PMID: 33953836 PMCID: PMC8057896 DOI: 10.1155/2021/6663948] [Citation(s) in RCA: 5] [Impact Index Per Article: 1.3] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Download PDF] [Figures] [Subscribe] [Scholar Register] [Received: 11/26/2020] [Revised: 02/14/2021] [Accepted: 04/02/2021] [Indexed: 11/17/2022]
Abstract
OBJECTIVE To explore the association between EAT volume and plaque precise composition and high risk plaque detected by coronary computed tomography angiography (CCTA). METHODS 101 patients with suspected coronary artery disease (CAD) underwent CCTA examination from March to July 2019 were enrolled, including 70 cases acute coronary syndrome (ACS) and 31 cases stable angina pectoris (SAP). Based on CCTA image, atherosclerotic plaque precise compositions were analyzed using dedicated quantitative software. High risk plaque was defined as plaque with more than 2 high risk features (spotty calcium, positive remolding, low attenuation plaque, napkin-ring sign) on CCTA image. The association between EAT volume and plaque composition was assessed as well as the different of correlation between ACS and SAP was analyzed. Multivariable logistic regression analysis was used to explore whether EAT volume was independent risk factors of high risk plaque (HRP). RESULTS EAT volume in the ACS group was significantly higher than that of the SAP group (143.7 ± 49.8 cm3 vs. 123.3 ± 39.2 cm3, P = 0.046). EAT volume demonstrated a significant positive correlation with total plaque burden (r = 0.298, P = 0.003), noncalcified plaque burden (r = 0.245, P = 0.013), lipid plaque burden (r = 0.250, P = 0.012), and homocysteine (r = 0.413, P ≤ 0.001). In ACS, EAT volume was positively correlated with total plaque burden (r = 0.309, P = 0.009), noncalcified plaque burden (r = 0.242, P = 0.044), and lipid plaque burden (r = 0.240, P = 0.045); however, no correlation was observed in SAP. Patients with HRP have larger EAT volume than those without HRP (169 ± 6.2 cm3 vs. 130.6 ± 5.3 cm3, P = 0.002). After adjustment by traditional risk factors and coronary artery calcium score (CACS), EAT volume was an independent risk predictor of presence of HRP (OR: 1.018 (95% CI: 1.006-1.030), P = 0.004). CONCLUSIONS With the increasing EAT volume, more dangerous plaque composition burdens increase significantly. EAT volume is a risk predictor of HRP independent of convention cardiovascular risk factors and CACS, which supports the potential impact of EAT on progression of coronary atherosclerotic plaque.
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Affiliation(s)
- Dongkai Shan
- Department of Cardiovascular Medicine, Sixth Medical Center, Chinese PLA General Hospital, Beijing, China
| | - Guanhua Dou
- Department of Cardiology, Second Medical Center, Chinese PLA General Hospital, Beijing, China
| | - Junjie Yang
- Department of Cardiovascular Medicine, Sixth Medical Center, Chinese PLA General Hospital, Beijing, China
| | - Xi Wang
- Department of Cardiology, First Medical Center, Chinese PLA General Hospital, Beijing, China
| | - Jingjing Wang
- Department of Cardiology, First Medical Center, Chinese PLA General Hospital, Beijing, China
| | - Wei Zhang
- Department of Cardiology, First Medical Center, Chinese PLA General Hospital, Beijing, China
| | - Bai He
- Department of Cardiology, First Medical Center, Chinese PLA General Hospital, Beijing, China
| | - Yuqi Liu
- Department of Cardiovascular Medicine, Sixth Medical Center, Chinese PLA General Hospital, Beijing, China
| | - Yundai Chen
- Department of Cardiovascular Medicine, Sixth Medical Center, Chinese PLA General Hospital, Beijing, China
| | - Yang Li
- Department of Cardiovascular Medicine, Sixth Medical Center, Chinese PLA General Hospital, Beijing, China
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