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Trandafir MF, Savu OI, Gheorghiu M. The Complex Immunological Alterations in Patients with Type 2 Diabetes Mellitus on Hemodialysis. J Clin Med 2024; 13:3687. [PMID: 38999253 PMCID: PMC11242658 DOI: 10.3390/jcm13133687] [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: 05/04/2024] [Revised: 06/14/2024] [Accepted: 06/23/2024] [Indexed: 07/14/2024] Open
Abstract
It is widely known that diabetes mellitus negatively impacts both the innate immunity (the inflammatory response) and the acquired immunity (the humoral and cellular immune responses). Many patients with diabetes go on to develop chronic kidney disease, which will necessitate hemodialysis. In turn, long-term chronic hemodialysis generates an additional chronic inflammatory response and impairs acquired immunity. The purpose of this paper is to outline and compare the mechanisms that are the basis of the constant aggression towards self-components that affects patients with diabetes on hemodialysis, in order to find possible new therapeutic ways to improve the functionality of the immune system. Our study will take a detailed look at the mechanisms of endothelial alteration in diabetes and hemodialysis, at the mechanisms of inflammatory generation and signaling at different levels and also at the mechanisms of inflammation-induced insulin resistance. It will also discuss the alterations in leukocyte chemotaxis, antigen recognition and the dysfunctionalities in neutrophils and macrophages. Regarding acquired immunity, we will outline the behavioral alterations of T and B lymphocytes induced by diabetes mellitus and chronic hemodialysis.
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Affiliation(s)
- Maria-Florina Trandafir
- Pathophysiology and Immunology Department, “Carol Davila” University of Medicine and Pharmacy, 020021 Bucharest, Romania;
- Doctoral School, “Carol Davila” University of Medicine and Pharmacy, 020021 Bucharest, Romania;
| | - Octavian Ionel Savu
- Doctoral School, “Carol Davila” University of Medicine and Pharmacy, 020021 Bucharest, Romania;
- “N. C. Paulescu” National Institute of Diabetes, Nutrition and Metabolic Diseases, 020475 Bucharest, Romania
| | - Mihaela Gheorghiu
- Pathophysiology and Immunology Department, “Carol Davila” University of Medicine and Pharmacy, 020021 Bucharest, Romania;
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Srikanth M, Rasool M. Resistin - A Plausible Therapeutic Target in the Pathogenesis of Psoriasis. Immunol Invest 2024; 53:115-159. [PMID: 38054436 DOI: 10.1080/08820139.2023.2288836] [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: 12/07/2023]
Abstract
Resistin, a cytokine hormone predominantly secreted by adipose tissue, is elevated in various metabolic disorders such as obesity, type 2 diabetes, and cardiovascular disease. In addition to its involvement in metabolic regulation, resistin has been implicated in the pathogenesis of psoriasis, a chronic inflammatory skin disorder. Numerous studies have reported increased resistin levels in psoriatic skin lesions, suggesting a possible association between resistin and psoriasis. Recent studies have suggested the potential involvement of resistin in the development and progression of certain cancers. Resistin is overexpressed in breast, colorectal, and gastric cancers. This suggests that it may play a role in the development of these cancers, possibly by inducing inflammation and cell growth. The link between resistin and cancer raises the possibility of shared underlying mechanisms driving the pathogenesis of psoriasis. Chronic inflammation, one such mechanism, is a hallmark of psoriasis and cancer. Further research is needed to fully understand the relationship between resistin and psoriasis. Identifying potential therapeutic targets is crucial for effective management of psoriasis. By doing so, we may be able to develop more effective treatment options for individuals living with psoriasis and ultimately improve their quality of life. Ultimately, a more comprehensive understanding of the mechanisms underlying the impact of resistin on psoriasis is essential for advancing our knowledge and finding new ways to treat and manage this challenging condition.
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Affiliation(s)
- Manupati Srikanth
- Immunopathology Lab, School of Biosciences and Technology, Vellore Institute of Technology (VIT), Vellore, India
| | - Mahaboobkhan Rasool
- Immunopathology Lab, School of Biosciences and Technology, Vellore Institute of Technology (VIT), Vellore, India
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Jbrael YJ, Hamad BK. Ameliorating impact of coenzyme Q10 on the profile of adipokines, cardiomyopathy, and hematological markers correlated with the glucotoxicity sequelae in diabetic rats. PLoS One 2024; 19:e0296775. [PMID: 38227584 PMCID: PMC10790996 DOI: 10.1371/journal.pone.0296775] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 07/25/2022] [Accepted: 12/18/2023] [Indexed: 01/18/2024] Open
Abstract
BACKGROUND In diabetes, high blood glucose induces glucotoxicity, resulting in the further damage of pancreatic beta-cells and then precipitating diabetic complications. This study was aimed to investigate the relationship between glucotoxicity with the level of adipokines, diabetic cardiomyopathy, and hematological markers. Moreover, the study examined the potential modulatory effect of coenzyme Q10 (CoQ10) on the aforementioned markers associated with the sequelae of diabetes mellitus. MATERIAL AND METHODS Twenty-four male rats were randomly assigned to receive an injection of STZ to induce diabetes (n = 16) or to remain uninduced (n = 8). The hyperglycemic status was induced in fasting rats by single intraperitoneal injection of STZ (45 mg /kg b.w.) dissolved in citrate buffer (pH 4.5). Three days after STZ injection, rats were divided into three groups; Normal control group (A), Diabetic control group (B), and CoQ10- treated diabetic group (C). The group (C) was fed with the basal diet supplemented with 5 g of CoQ10 per kilogram of diet for three weeks after the diabetes induction. After 21 days, the blood and serum samples were taken to conduct biochemical analyses. Blood glucose was determined by Blood Glucose Monitoring System. Adipokines or cytokines were evaluated by ELISA from a serum sample. Cardiac myopathy biomarkers were estimated by UP-Converting Phosphor Immunoassay Analyzer, and hematological parameters were measured by automatic hematology analyzer. RESULTS In hyperglycemic rats, the level of fasting blood glucose, and serum level of resistin, omentin, TNF-α, and cardiomyopathy biomarkers significantly increased (P < 0.05). The treatment with CoQ10 significantly decreased the profile of adipokines and cardiomyopathy markers (cardiac enzymes and LPPLA2) in diabetic rats and also reduced glucose levels (P < 0.05). Lymphocyte percentages significantly decreased while significant increases were observed in granulocytes and MID percentages in hyperglycemic rats. CONCLUSION Diabetic rats had higher serum levels of adipokines and cardiomyopathy markers. Among the hematological markers, GRA% and MID% increased while LYM% decreased. The profile of adipokines and cardiomyopathy markers improved when CoQ10 was supplemented. The study suggests that CoQ10 may have a beneficial effect on improving diabetic complications.
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Affiliation(s)
- Yousif Jameel Jbrael
- Department of Pharmacology and Toxicology, College of Pharmacy, Hawler Medical University, Erbil, Iraq
| | - Badraldin Kareem Hamad
- Department of Pharmacology and Toxicology, College of Pharmacy, Hawler Medical University, Erbil, Iraq
- University of Kurdistan Hawler (UKH), School of Medicine, Erbil, Iraq
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Stakhneva EM, Kuzminykh NA, Scherbakova LV, Kashtanova EV, Polonskaya YV, Shramko VS, Garbuzova Striukova EV, Sadovski EV, Ragino YI. Metabolic Blood Hormones in Young People With Electrocardiographic Signs of Ischemic Myocardial Changes. KARDIOLOGIIA 2023; 63:4-11. [PMID: 38088107 DOI: 10.18087/cardio.2023.11.n2492] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Subscribe] [Scholar Register] [Received: 04/21/2023] [Revised: 07/10/2023] [Accepted: 07/27/2023] [Indexed: 12/18/2023]
Abstract
Aim To study changes in blood concentrations of metabolic hormones and adipocytokines in people aged 25-44 years with electrocardiographic (ECG) signs of ischemic changes in the myocardium.Material and methods This study was a part of a cross-sectional survey of a random sample of Novosibirsk population aged 25-44 years. The study included 1363 people divided into two groups: group 1, subjects with ECG signs of ischemic changes in the myocardium and group 2, subjects without ECG changes. Blood serum concentrations of adipocytokines and metabolic hormones were measured by multiplex assay on a Luminex MAGPIX flow-through fluorometer.Results The group with ECG signs of myocardial ischemia had higher blood concentrations of adiponectin, resistin, glucagon, and interleukin 6 (IL-6) than in the comparison group. A multivariate logistic regression analysis showed that the glucagon concentration was associated with the presence of ECG signs of myocardial ischemia (OR, 1.019; CI, 1.018-1.034; p=0.017).Conclusion In young people aged 25-44 years, higher blood concentrations of glucagon are associated with the presence of ECG signs of myocardial ischemia.
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Affiliation(s)
- E M Stakhneva
- Research Institute of Therapy and Preventive Medicine, Branch of the Federal Research Center Institute of Cytology and Genetics, Siberian Branch of the Russian Academy of Sciences
| | - N A Kuzminykh
- Research Institute of Therapy and Preventive Medicine, Branch of the Federal Research Center Institute of Cytology and Genetics, Siberian Branch of the Russian Academy of Sciences
| | - L V Scherbakova
- Research Institute of Therapy and Preventive Medicine, Branch of the Federal Research Center Institute of Cytology and Genetics, Siberian Branch of the Russian Academy of Sciences
| | - E V Kashtanova
- Research Institute of Therapy and Preventive Medicine, Branch of the Federal Research Center Institute of Cytology and Genetics, Siberian Branch of the Russian Academy of Sciences
| | - Ya V Polonskaya
- Research Institute of Therapy and Preventive Medicine, Branch of the Federal Research Center Institute of Cytology and Genetics, Siberian Branch of the Russian Academy of Sciences
| | - V S Shramko
- Research Institute of Therapy and Preventive Medicine, Branch of the Federal Research Center Institute of Cytology and Genetics, Siberian Branch of the Russian Academy of Sciences
| | - E V Garbuzova Striukova
- Research Institute of Therapy and Preventive Medicine, Branch of the Federal Research Center Institute of Cytology and Genetics, Siberian Branch of the Russian Academy of Sciences
| | - E V Sadovski
- Research Institute of Therapy and Preventive Medicine, Branch of the Federal Research Center Institute of Cytology and Genetics, Siberian Branch of the Russian Academy of Sciences
| | - Yu I Ragino
- Research Institute of Therapy and Preventive Medicine, Branch of the Federal Research Center Institute of Cytology and Genetics, Siberian Branch of the Russian Academy of Sciences
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Mitidieri E, Turnaturi C, Vanacore D, Sorrentino R, d'Emmanuele di Villa Bianca R. The Role of Perivascular Adipose Tissue-Derived Hydrogen Sulfide in the Control of Vascular Homeostasis. Antioxid Redox Signal 2022; 37:84-97. [PMID: 35442088 DOI: 10.1089/ars.2021.0147] [Citation(s) in RCA: 5] [Impact Index Per Article: 1.7] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 12/25/2022]
Abstract
Significance: Emerging evidence suggests that perivascular adipose tissue (PVAT) has a relevant role in the control of vascular tone in physiology and pathology. Healthy PVAT has anticontractile, anti-inflammatory, and antioxidative actions. Accumulating data from both human and experimental animal models indicate that PVAT dysfunction is conceivably coupled to cardiovascular diseases, and it is associated with vascular inflammation, oxidative stress, and arterial remodeling. Therefore, "healthy" PVAT may constitute a novel therapeutic target for the prevention and treatment of cardiovascular diseases. Recent Advances: Hydrogen sulfide (H2S) has been recognized as a vascular anti-contractile factor released from PVAT. The enzymes deputed to H2S biosynthesis are variously expressed in PVAT and strictly dependent on the vascular bed and species. Metabolic and cardiovascular diseases can alter the morphological and secretory characteristics of PVAT, influencing also the H2S signaling. Here, we discuss the role of PVAT-derived H2S in healthy conditions and its relevance in alterations occurring in vascular disorders. Critical Issues: We discuss how a better understanding may help in the prevention of vascular dysfunction related to alteration in PVAT-released H2S as well as the importance of the interplay between PVAT and H2S. Future Directions: We propose future directions to evaluate the contribution of each enzyme involved in H2S biosynthesis and their alteration/switch occurring in vascular disorders and the remaining challenges in investigating the role of H2S. Antioxid. Redox Signal. 37, 84-97.
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Affiliation(s)
- Emma Mitidieri
- Department of Pharmacy, School of Medicine and Surgery, University of Naples Federico II, Naples, Italy
| | - Carlotta Turnaturi
- Department of Pharmacy, School of Medicine and Surgery, University of Naples Federico II, Naples, Italy
| | - Domenico Vanacore
- Department of Pharmacy, School of Medicine and Surgery, University of Naples Federico II, Naples, Italy
| | - Raffaella Sorrentino
- Department of Molecular Medicine and Medical Biotechnology, School of Medicine, University of Naples Federico II, Naples, Italy
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Zhang P, Chen K, He T, Guo H, Chen X. Coenzyme Q10 supplementation improves adipokine profile in dyslipidemic individuals: a randomized controlled trial. Nutr Metab (Lond) 2022; 19:13. [PMID: 35241098 PMCID: PMC8896379 DOI: 10.1186/s12986-022-00649-5] [Citation(s) in RCA: 3] [Impact Index Per Article: 1.0] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 10/05/2021] [Accepted: 02/15/2022] [Indexed: 11/10/2022] Open
Abstract
Background In previous study, we found that coenzyme Q10 (CoQ10) improved glucolipid profile in dyslipidemic individuals, but the mechanism is not yet clear. Adipokines have been demonstrated to be vital targets of metabolic diseases. The hypothesis that adipokines mediate the association of CoQ10 on glucolipid metabolism needs to be further studied in human. Methods In this randomized, double-blinded, placebo-controlled trial, 101 dyslipidemic individuals were administrated to 120 mg CoQ10 or placebo for 24 weeks. Anthropometric parameters, glucolipid profile, serum total adiponectin, leptin, and resistin were evaluated at baseline, week 12 and week 24. Results CoQ10 treatment significantly increased serum adiponectin levels at week 12 (165 [0, 362] ng/mL, p < 0.001) and at week 24 (523 [0, 1056] ng/mL, p < 0.001]), which was significant different compared with placebo (p < 0.001). The increase of adiponectin was negative associated with decrease in index of homeostasis model assessment of insulin resistance (HOMA-IR, r = − 0.465, p = 0.001), triglyceride (TG, r = − 0.297, p = 0.047), and low-density lipoprotein cholesterol (LDL-c, r = − 0.440, p = 0.002) at week 24 only in CoQ10-treated group. Resistin was reduced by CoQ10 only at week 24 (− 1.19 [− 4.35, 0.00] ng/mL, p < 0.001), which was significant different compared with placebo (p < 0.001). Reduction of resistin was positively correlated with the change in HOMA-IR (r = 0.343, p = 0.021) and TG (r = 0.323, p = 0.030) at week 24 in CoQ10-treated group but not placebo group. Leptin was not influenced by CoQ10 treatment. Mediation analysis indicated that the improvement of HOMA-IR, TG and LDL-c by CoQ10 was mediated by adiponectin but not resistin. Conclusions Our study shows that CoQ10 ameliorates glucolipid profile and adipokines dysfunction in dyslipidemic patients in 24 weeks’ intervention. The beneficial effect of CoQ10 on glucolipid profile was mediated by adiponectin. Trial registration: ClinicalTrials.gov, NCT02407548. Registered on April 3, 2015, https://clinicaltrials.gov/ct2/show/NCT02407548. Supplementary Information The online version contains supplementary material available at 10.1186/s12986-022-00649-5.
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Affiliation(s)
- Peiwen Zhang
- Department of Nutrition, School of Public Health, Guangdong Medical University, Dongguan, People's Republic of China.,School of Public Health, Dongguan Key Laboratory of Environmental Medicine, Guangdong Medical University, Dongguan, People's Republic of China
| | - Ke Chen
- Department of Nutrition, School of Public Health, Sun Yat-Sen University, Guangzhou, People's Republic of China
| | - Taiping He
- Department of Nutrition, School of Public Health, Guangdong Medical University, Dongguan, People's Republic of China.,School of Public Health, Dongguan Key Laboratory of Environmental Medicine, Guangdong Medical University, Dongguan, People's Republic of China
| | - Honghui Guo
- Department of Nutrition, School of Public Health, Guangdong Medical University, Dongguan, People's Republic of China. .,School of Public Health, Dongguan Key Laboratory of Environmental Medicine, Guangdong Medical University, Dongguan, People's Republic of China.
| | - Xu Chen
- Department of Nutrition, School of Public Health, Guangdong Medical University, Dongguan, People's Republic of China. .,Department of Nutrition, School of Public Health, Sun Yat-Sen University, Guangzhou, People's Republic of China.
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Scărlătescu AI, Micheu MM, Popa-Fotea N, Pascal AM, Mihail AM, Petre I, Deaconu S, Vîjîiac A, Dorobanțu M. IL-6, IL-1RA and Resistin as Predictors of Left Ventricular Remodelling and Major Adverse Cardiac Events in Patients with Acute ST Elevation Myocardial Infarction. Diagnostics (Basel) 2022; 12:266. [PMID: 35204357 PMCID: PMC8871243 DOI: 10.3390/diagnostics12020266] [Citation(s) in RCA: 5] [Impact Index Per Article: 1.7] [Reference Citation Analysis] [Abstract] [Key Words] [Grants] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 12/21/2021] [Revised: 01/12/2022] [Accepted: 01/17/2022] [Indexed: 12/14/2022] Open
Abstract
Despite continuous advances in diagnostic and therapeutic methods, acute myocardial infarction (AMI) remains a leading cause of morbidity and mortality worldwide. Considering the role of inflammation in AMI etiopathogenesis, we aimed to explore the role of a group of three inflammatory cytokines (IL-1RA, IL-6 and resistin) as an independent prognostic factor for LVR assessed by 3D echocardiography and MACE in patients with STEMI. We enrolled 41 patients with STEMI who underwent primary PCI. We assessed the occurrence of LVR (defined as an increase of over 20% in end-diastolic left ventricular volume at 6 months compared with baseline values) and MACE. Using the enzyme-linked immunosorbent assays (ELISA) method, we measured plasmatic levels of IL-6, IL-1RA and resistin (within 48 h after AMI and at 6 months). Out of 41 STEMI patients, 20.5% presented signs of LVR at follow up, and in 24.4%, MACE occurred. In univariate logistic regression analysis, baseline levels of IL-6 (OR = 1.042, p = 0.004), IL-1RA (OR = 1.004, p = 0.05) and resistin (OR = 1.7, p = 0.007) were all significantly associated with LVR. ROC analysis showed that the three cytokines as a group (AUC 0.946, p = 0.000) have a better predictive value for LVR than any individual cytokine. The group of cytokines also proved to have a better predictive value for MACE together than separately (AUC = 0.875, p = 0.000 for ROC regression model). IL-6, IL-1RA and resistin plasma levels at baseline have a good predictive value both as independent variables and also as a group for the development of adverse LVR and MACE at 6 months follow up after STEMI.
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Affiliation(s)
- Alina Ioana Scărlătescu
- Department of Cardiology, “Carol Davila” University of Medicine and Pharmacy, 050474 Bucharest, Romania; (A.I.S.); (N.P.-F.); (I.P.); (A.V.); (M.D.)
- Emergency Clinical Hospital Bucharest, Department of Cardiology, 014461 Bucharest, Romania; (A.M.P.); (A.M.M.); (S.D.)
| | - Miruna Mihaela Micheu
- Emergency Clinical Hospital Bucharest, Department of Cardiology, 014461 Bucharest, Romania; (A.M.P.); (A.M.M.); (S.D.)
| | - Nicoleta Popa-Fotea
- Department of Cardiology, “Carol Davila” University of Medicine and Pharmacy, 050474 Bucharest, Romania; (A.I.S.); (N.P.-F.); (I.P.); (A.V.); (M.D.)
- Emergency Clinical Hospital Bucharest, Department of Cardiology, 014461 Bucharest, Romania; (A.M.P.); (A.M.M.); (S.D.)
| | - Ana Maria Pascal
- Emergency Clinical Hospital Bucharest, Department of Cardiology, 014461 Bucharest, Romania; (A.M.P.); (A.M.M.); (S.D.)
| | - Ana Maria Mihail
- Emergency Clinical Hospital Bucharest, Department of Cardiology, 014461 Bucharest, Romania; (A.M.P.); (A.M.M.); (S.D.)
| | - Ioana Petre
- Department of Cardiology, “Carol Davila” University of Medicine and Pharmacy, 050474 Bucharest, Romania; (A.I.S.); (N.P.-F.); (I.P.); (A.V.); (M.D.)
- Emergency Clinical Hospital Bucharest, Department of Cardiology, 014461 Bucharest, Romania; (A.M.P.); (A.M.M.); (S.D.)
| | - Silvia Deaconu
- Emergency Clinical Hospital Bucharest, Department of Cardiology, 014461 Bucharest, Romania; (A.M.P.); (A.M.M.); (S.D.)
| | - Aura Vîjîiac
- Department of Cardiology, “Carol Davila” University of Medicine and Pharmacy, 050474 Bucharest, Romania; (A.I.S.); (N.P.-F.); (I.P.); (A.V.); (M.D.)
- Emergency Clinical Hospital Bucharest, Department of Cardiology, 014461 Bucharest, Romania; (A.M.P.); (A.M.M.); (S.D.)
| | - Maria Dorobanțu
- Department of Cardiology, “Carol Davila” University of Medicine and Pharmacy, 050474 Bucharest, Romania; (A.I.S.); (N.P.-F.); (I.P.); (A.V.); (M.D.)
- Emergency Clinical Hospital Bucharest, Department of Cardiology, 014461 Bucharest, Romania; (A.M.P.); (A.M.M.); (S.D.)
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Diaz-Canestro C, Xu A. Impact of Different Adipose Depots on Cardiovascular Disease. J Cardiovasc Pharmacol 2021; 78:S30-S39. [PMID: 34840259 DOI: 10.1097/fjc.0000000000001131] [Citation(s) in RCA: 2] [Impact Index Per Article: 0.5] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 06/15/2021] [Accepted: 08/05/2021] [Indexed: 12/13/2022]
Abstract
ABSTRACT Adipose tissue (AT)-derived factors contribute to the regulation of cardiovascular homeostasis, thereby playing an important role in cardiovascular health and disease. In obesity, AT expands and becomes dysfunctional, shifting its secretory profile toward a proinflammatory state associated with deleterious effects on the cardiovascular system. AT in distinct locations (ie, adipose depots) differs in crucial phenotypic variables, including inflammatory and secretory profile, cellular composition, lipolytic activity, and gene expression. Such heterogeneity among different adipose depots may explain contrasting cardiometabolic risks associated with different obesity phenotypes. In this respect, central obesity, defined as the accumulation of AT in the abdominal region, leads to higher risk of cardiometabolic alterations compared with the accumulation of AT in the gluteofemoral region (ie, peripheral obesity). The aim of this review was to provide an updated summary of clinical and experimental evidence supporting the differential roles of different adipose depots in cardiovascular disease and to discuss the molecular basis underlying the differences of adipose depots in the regulation of cardiovascular function.
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Affiliation(s)
- Candela Diaz-Canestro
- State Key Laboratory of Pharmaceutical Biotechnology, the University of Hong Kong, Hong Kong, China
- Department of Medicine, the University of Hong Kong, Hong Kong, China; and
| | - Aimin Xu
- State Key Laboratory of Pharmaceutical Biotechnology, the University of Hong Kong, Hong Kong, China
- Department of Medicine, the University of Hong Kong, Hong Kong, China; and
- Department of Pharmacology and Pharmacy, the University of Hong Kong, Hong Kong, China
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Palla G, Ramírez-Morán C, Montt-Guevara MM, Salazar-Pousada D, Shortrede J, Simoncini T, Grijalva-Grijalva I, Pérez-López FR, Chedraui P. Perimenopause, body fat, metabolism and menopausal symptoms in relation to serum markers of adiposity, inflammation and digestive metabolism. J Endocrinol Invest 2020; 43:809-820. [PMID: 31925754 DOI: 10.1007/s40618-019-01168-6] [Citation(s) in RCA: 10] [Impact Index Per Article: 2.0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 10/12/2019] [Accepted: 12/19/2019] [Indexed: 01/22/2023]
Abstract
BACKGROUND Perimenopausal women gain weight that may alter inflammatory status, endocrine equilibrium, and the intensity of vasomotor symptoms. OBJECTIVE To measure serum levels of markers related to adiposity, inflammation/angiogenesis and digestive metabolism and correlate them with body mass index (BMI), waist-to-hip ratio (WHR), metabolic parameters and menopausal symptoms (assessed with the 10-item Cervantes Scale [CS-10]). METHODS Serum of perimenopausal women (n = 24), STRAW stages-2 and -1, was analyzed using the Bio-Plex 200 System technology to assess 30 proposed analytes. The MetS was defined by the American Heart Association criteria and women were divided as: normal BMI (NBMI), excessive BMI (EBMI), and EBMI with MetS (EBMI-MetS). RESULTS Weight, BMI, abdominal circumference, WHR, systolic blood pressure, glucose and triglyceride levels were significantly higher and high-density lipoprotein cholesterol (HDL-C) was lower in EBMI-MetS women compared to NBMI ones. Insulin, C-peptide, resistin, adipsin, GIP, leptin, IL-6, FGF21 and PAI-1 levels were significantly higher and ghrelin and IGFBP-1 lower in EBMI-MetS women as compared to NBMI ones. Spearman's correlation of pooled data showed a significant positive correlation between abdominal perimeter and WHR and C-peptide, insulin, adipsin, resistin, leptin, PAI-1 and FGF21 and a negative correlation with IGFBP-1 levels. Total CS-10 scores and hot flush intensity did not differ between studied groups, yet positively correlated with anthropometric values but not with studied analytes. CONCLUSION Perimenopausal women with EBMI and the MetS showed an altered metabolic profile, but no differences in menopausal symptoms which also did not correlate with changes in studied biomarkers.
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Affiliation(s)
- G Palla
- Division of Obstetrics and Gynecology, Department of Clinical and Experimental Medicine, University of Pisa, Pisa, Italy
| | - C Ramírez-Morán
- Instituto de Investigación e Innovación en Salud Integral, Facultad de Ciencias Médicas, Universidad Católica de Santiago de Guayaquil, Guayaquil, Ecuador
| | - M M Montt-Guevara
- Division of Obstetrics and Gynecology, Department of Clinical and Experimental Medicine, University of Pisa, Pisa, Italy
| | - D Salazar-Pousada
- Instituto de Investigación e Innovación en Salud Integral, Facultad de Ciencias Médicas, Universidad Católica de Santiago de Guayaquil, Guayaquil, Ecuador
| | - J Shortrede
- Division of Obstetrics and Gynecology, Department of Clinical and Experimental Medicine, University of Pisa, Pisa, Italy
| | - T Simoncini
- Division of Obstetrics and Gynecology, Department of Clinical and Experimental Medicine, University of Pisa, Pisa, Italy.
| | - I Grijalva-Grijalva
- Instituto de Investigación e Innovación en Salud Integral, Facultad de Ciencias Médicas, Universidad Católica de Santiago de Guayaquil, Guayaquil, Ecuador
| | - F R Pérez-López
- Red de Investigación de Obstetricia, Ginecología y Reproducción, Instituto de Investigaciones Sanitarias de Aragón, University of Zaragoza, Faculty of Medicine, Zaragoza, Spain
| | - P Chedraui
- Instituto de Investigación e Innovación en Salud Integral, Facultad de Ciencias Médicas, Universidad Católica de Santiago de Guayaquil, Guayaquil, Ecuador.
- Facultad de Ciencias de la Salud, Universidad Católica "Nuestra Señora de la Asunción", Asunción, Paraguay.
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Influence of +299G>A and +62G˃A resistin gene promoter variants on cardiovascular risk in Egyptian women with systemic lupus erythematosus. EGYPTIAN RHEUMATOLOGIST 2019. [DOI: 10.1016/j.ejr.2018.11.005] [Citation(s) in RCA: 5] [Impact Index Per Article: 0.8] [Reference Citation Analysis] [Track Full Text] [Subscribe] [Scholar Register] [Indexed: 12/23/2022]
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11
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Acquarone E, Monacelli F, Borghi R, Nencioni A, Odetti P. Resistin: A reappraisal. Mech Ageing Dev 2019; 178:46-63. [DOI: 10.1016/j.mad.2019.01.004] [Citation(s) in RCA: 51] [Impact Index Per Article: 8.5] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 08/08/2018] [Revised: 12/28/2018] [Accepted: 01/11/2019] [Indexed: 02/07/2023]
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Zhang P, Liu Y, Su J, Bai J, Zhao S, Zhao S. Resistin impairs activation of protein C by suppressing EPCR and increasing SP1 expression. Biomed Pharmacother 2019; 109:930-937. [PMID: 30551547 DOI: 10.1016/j.biopha.2018.09.160] [Citation(s) in RCA: 3] [Impact Index Per Article: 0.5] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 04/08/2018] [Revised: 09/27/2018] [Accepted: 09/28/2018] [Indexed: 11/25/2022] Open
Abstract
Endothelial cells are vital to blood coagulation and maintain whole body hemostasis. Binding of endothelial cells to endothelial protein C receptor (EPCR) and thrombomodulin (TM) is essential to the formation of activated protein C (APC), one of the key factors regulating blood coagulation. In our study, we showed that resistin, an adipocyte hormone, suppresses thrombin-induced protein C activation in endothelial cells. Resistin treatment results in a reduction in EPCR expression, but not TM. Mechanistically, we demonstrate that resistin induces expression of the nuclear transcription factor SP-1, which could lead to downregulation of EPCR. Both inhibition and silencing of SP1 protein abolishes abnormal APC generation induced by resistin. Collectively, our data support a new role of resistin in disturbing APC formation.
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Affiliation(s)
- Pei Zhang
- Department of Endocrinology, Liaocheng People's Hospital, Liaocheng 252000, China
| | - Yu Liu
- Department of Endocrinology, Liaocheng People's Hospital, Liaocheng 252000, China
| | - Jiangli Su
- Department of Neurology, Liaocheng People's Hospital, NO.67 Dongchang West Road, Liaocheng 252000, China.
| | - Jie Bai
- Department of Endocrinology, Liaocheng People's Hospital, Liaocheng 252000, China
| | - Shikai Zhao
- Department of Andrology, Liaocheng People's Hospital, Liaocheng 252000, China
| | - Shouguo Zhao
- Department of Andrology, Liaocheng People's Hospital, Liaocheng 252000, China
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Lu Y, Monaco G, Camous X, Andiappan AK, Rotzschke O, Ng TP, Larbi A. Biomarker Signatures Predicting 10-Year All-Cause and Disease-Specific Mortality. J Gerontol A Biol Sci Med Sci 2018; 74:469-479. [DOI: 10.1093/gerona/gly138] [Citation(s) in RCA: 6] [Impact Index Per Article: 0.9] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 02/11/2018] [Indexed: 01/21/2023] Open
Affiliation(s)
- Yanxia Lu
- Singapore Immunology Network (SIgN), Agency for Science Technology and Research (A*STAR), Biopolis, Singapore
| | - Gianni Monaco
- Institute of Ageing and Chronic Disease, University of Liverpool, UK
| | - Xavier Camous
- Singapore Immunology Network (SIgN), Agency for Science Technology and Research (A*STAR), Biopolis, Singapore
| | - Anand Kumar Andiappan
- Singapore Immunology Network (SIgN), Agency for Science Technology and Research (A*STAR), Biopolis, Singapore
| | - Olaf Rotzschke
- Singapore Immunology Network (SIgN), Agency for Science Technology and Research (A*STAR), Biopolis, Singapore
| | - Tze Pin Ng
- Gerontology Research Programme, Department of Psychological Medicine, National University Health System, Yong Loo Lin School of Medicine, National University of Singapore, Singapore
| | - Anis Larbi
- Singapore Immunology Network (SIgN), Agency for Science Technology and Research (A*STAR), Biopolis, Singapore
- Department of Biology, Faculty of Science, University Tunis El Manar, Tunis, Tunisia
- Geriatrics Division, Department of Medicine, Research Center on Ageing, University of Sherbrooke, Quebec, Canada
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14
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Association between Two Resistin Gene Polymorphisms and Metabolic Syndrome in Jilin, Northeast China: A Case-Control Study. DISEASE MARKERS 2018; 2017:1638769. [PMID: 29386698 PMCID: PMC5745751 DOI: 10.1155/2017/1638769] [Citation(s) in RCA: 2] [Impact Index Per Article: 0.3] [Reference Citation Analysis] [Abstract] [Track Full Text] [Download PDF] [Subscribe] [Scholar Register] [Received: 07/26/2017] [Revised: 10/17/2017] [Accepted: 10/30/2017] [Indexed: 12/12/2022]
Abstract
Metabolic syndrome (MetS) is a significant health care problem worldwide and is characterized by increased fasting glucose and obesity. Resistin is a protein hormone produced both by adipocytes and immunocompetent cells, including those residing in adipose tissue, and is believed to modulate glucose tolerance and insulin action. This study examined the association of resistin gene polymorphisms, rs1862513 and rs3745368, and related haplotypes with the development of metabolic syndrome in a Han Chinese population. This case-control study was performed on 3792 subjects, including 1771 MetS cases and 2021 healthy controls from the Jilin province of China. Metabolic syndrome was defined according to the criteria of the International Diabetes Federation (IDF). Logistic regression analysis was used to estimate the relationship between gene polymorphism and MetS. Our results showed that there were no significant associations between MetS and the genotype distributions in four kinds of inheritance models, allele frequencies, and related haplotypes of resistin gene polymorphisms rs1862513 and rs3745368 (all p values > 0.05). Based on our study findings, we concluded that mutations in resistin genes are not associated with the presence of MetS in a Han Chinese population from Jilin province in China.
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Zuniga MC, Raghuraman G, Zhou W. Physiologic levels of resistin induce a shift from proliferation to apoptosis in macrophage and VSMC co-culture. Surgery 2018; 163:906-911. [PMID: 29361366 DOI: 10.1016/j.surg.2017.10.051] [Citation(s) in RCA: 17] [Impact Index Per Article: 2.4] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 03/02/2017] [Revised: 09/26/2017] [Accepted: 10/28/2017] [Indexed: 10/18/2022]
Abstract
BACKGROUND Resistin, an adipokine with inflammatory properties, has been associated with plaque vulnerability. Vascular smooth muscle cells and macrophages are the major cellular components in advanced atherosclerotic plaques and interdependently affect plaque stability. The purpose of this study was to examine the effects of resistin on the interactions of vascular smooth muscle cells and macrophages using co-culture systems. METHODS Human monocytes were differentiated into macrophages. Vascular smooth muscle cells were grown and starved prior to co-culture condition. Indirect co-culture was performed by treating macrophages with resistin at 10 ng/mL for 24 hours with/without εV1-2, a selective protein kinase C epsilon inhibitor. Macrophages supernatants were then used to treat vascular smooth muscle cells for 24 hours. Direct co-culture was performed by culturing macrophages and vascular smooth muscle cells together for 24 to 48 hours. Cultures were evaluated for changes in proliferation, apoptosis, and gene expression of apoptosis, proliferation, and inflammation-associated genes. RESULTS Macrophages induced vascular smooth muscle cells proliferation, which was further exaggerated in resistin-treated macrophages in the indirect co-culture model. Resistin also upregulated cyclin D1 and proliferating cell nuclear antigen via protein kinase C epsilon in the indirect co-culture. Augmented proliferation was further confirmed in the direct co-culture model, particularly at increased macrophage ratios. However, resistin treatment induced apoptosis in the presence of direct cell to cell interactions. Along with the shift to apoptosis, expressions of caspase 3 and caspase 8 were upregulated. The expression of kappa-light-chain-enhancer of activated B cells 1 and 2 was similar in direct and indirect co-cultures. CONCLUSION Resistin promotes a shift from proliferation to apoptosis in vascular smooth muscle cells and macrophage co-culture systems with cellular composition similar to that found in vulnerable regions of plaques. Protein kinase C epsilon mediates the effects of resistin, suggesting that protein kinase C epsilon may represent a therapeutic strategy in resistin-associated atherosclerotic complications.
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Affiliation(s)
- Mary C Zuniga
- Department of Vascular Surgery, VA Palo Alto Health Care System, Palo Alto, CA, USA
| | - Gayatri Raghuraman
- Department of Vascular Surgery, VA Palo Alto Health Care System, Palo Alto, CA, USA
| | - Wei Zhou
- Division of Vascular Surgery, Department of Surgery, University of Arizona, Tucson, AZ, USA; Department of Vascular Surgery, Southern Arizona VA Health Care System, Tucson, AZ, USA.
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Munjas J, Sopić M, Spasojević-Kalimanovska V, Kalimanovska-Oštrić D, Anđelković K, Jelić-Ivanović Z. Association of adenylate cyclase-associated protein 1 with coronary artery disease. Eur J Clin Invest 2017; 47:659-666. [PMID: 28707728 DOI: 10.1111/eci.12787] [Citation(s) in RCA: 10] [Impact Index Per Article: 1.3] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 11/04/2016] [Accepted: 07/10/2017] [Indexed: 01/09/2023]
Abstract
BACKGROUND Adenylate cyclase-associated protein 1 (CAP1) is a recently identified receptor for human resistin. As resistin has been related to CAD development and progression and CAP1 has never been evaluated in CAD, the aim of this study was to determine its peripheral blood mononuclear cells (PBMCs) mRNA in patients with CAD, and resistin plasma concentration, PBMCs resistin and CD36 mRNA, considering resistiǹs ability to stimulate CD36 expression in vitro. MATERIALS AND METHODS This case-controlled study included 27 healthy subjects (CG) and 66 patients requiring coronary angiography. Of the latter, 42 had nonsignificant CAD whereas 24 had significant CAD. Circulating resistin was measured by ELISA; PBMCs CAP1, resistin and CD36 mRNA were determined by real-time PCR. RESULTS Patients with significant as well as patients with nonsignificant CAD had significantly higher resistin concentrations compared to the CG (P < 0·001; P = 0·003). Resistin mRNA did not show significant difference between the investigated groups. CAP1 and CD36 mRNA were significantly higher in significant CAD (P < 0·001; P < 0·001, respectively) and nonsignificant CAD (P < 0·001; P < 0·001, respectively) compared to the CG; significant CAD showed significantly higher CD36 mRNA (P = 0·040) compared to the nonsignificant CAD group. Multiple linear regression analysis identified Tg and CD36 mRNA as independent predictors of CAP1 (R2 = 0·402; adjR2 = 0·376). CONCLUSION Significant up-regulation of PBMCs CAP1, CD36 mRNA and plasma resistin found in significant CAD, as well as in nonsignificant CAD compared to CG, indicates that resistin could be able to exert its effects stronger on cells with up-regulated CAP1 mRNA thus contributing atherosclerosis development.
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Affiliation(s)
- Jelena Munjas
- Department of Medical Biochemistry, Faculty of Pharmacy, University of Belgrade, Belgrade, Serbia
| | - Miron Sopić
- Department of Medical Biochemistry, Faculty of Pharmacy, University of Belgrade, Belgrade, Serbia
| | | | - Dimitra Kalimanovska-Oštrić
- Institute for Cardiovascular Diseases, Clinical Center of Serbia, Belgrade, Serbia.,School of Medicine, University of Belgrade, Belgrade, Serbia
| | - Kristina Anđelković
- Institute for Cardiovascular Diseases, Clinical Center of Serbia, Belgrade, Serbia
| | - Zorana Jelić-Ivanović
- Department of Medical Biochemistry, Faculty of Pharmacy, University of Belgrade, Belgrade, Serbia
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17
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Lynch M, Ahern T, Sweeney CM, Malara A, Tobin AM, O'Shea D, Kirby B. Adipokines, psoriasis, systemic inflammation, and endothelial dysfunction. Int J Dermatol 2017; 56:1103-1118. [DOI: 10.1111/ijd.13699] [Citation(s) in RCA: 32] [Impact Index Per Article: 4.0] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 02/14/2017] [Revised: 05/06/2017] [Accepted: 06/09/2017] [Indexed: 12/11/2022]
Affiliation(s)
- Maeve Lynch
- St. Vincent's University Hospital; Dublin Ireland
| | - Tomas Ahern
- St. Vincent's University Hospital; Dublin Ireland
| | | | - Anna Malara
- St. Vincent's University Hospital; Dublin Ireland
| | | | - Donal O'Shea
- St. Vincent's University Hospital; Dublin Ireland
| | - Brian Kirby
- St. Vincent's University Hospital; Dublin Ireland
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18
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Zhang JZ, Gao Y, Zheng YY, Liu F, Yang YN, Li XM, Ma X, Ma YT, Xie X. Increased serum resistin level is associated with coronary heart disease. Oncotarget 2017; 8:50148-50154. [PMID: 28404934 PMCID: PMC5564838 DOI: 10.18632/oncotarget.15707] [Citation(s) in RCA: 16] [Impact Index Per Article: 2.0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 11/24/2016] [Accepted: 01/24/2017] [Indexed: 01/29/2023] Open
Abstract
To explore the relationship between the serum resistin level and different types of coronary heart diseases (CHD). Literature was retrieved by formal searching of PubMed, Web of Science, Google Scholar, the Cochrane Library, Wanfang Data, China Biological Medicine Database (SinoMed) and China National Knowledge Infrastructure (CNKI) and by hand searching of reference lists of related articles. RevMan5.3 statistical software was utilized for processing and analysis. A total of 22 literatures involving 2070 subjects were included. Meta-analysis showed that the level of serum resistin in the patients with stable angina (SA), unstable angina(UA) or acute myocardial infarction (AMI) were significantly higher than those of normal controls, respectively [SMD(95% CI)were 1.97(1.15, 2.79), 2.54(1.76, 3.31), and 3.62(2.62, 4.62), all P<0.00001]. Serum resistin level in patients with UA or AMI was higher than those in patients with SA, respectively [SMD=0.90, 95CI(0.28,1.52), P=0.005], [SMD=2.28, 95%CI(0.74, 3.82), P=0.004].The level of serum resistin in patients with AMI was also higher than those in patients with UA [SMD=1.22, 95%CI(0.58, 1.85), P=0.0002]. The study demonstrated that increased serum resistin level is significantly associated with the severity of CHD.
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Affiliation(s)
- Jing-Zhan Zhang
- Department of Cardiology, First Affiliated Hospital of Xinjiang Medical University, Urumqi, China
- Department of Dermatology, People's Hospital of Xinjiang Uygur Autonomous Region, Urumqi, China
| | - Ying Gao
- Department of Cadre Ward, First Affiliated Hospital of Xinjiang Medical University, Urumqi, China
| | - Ying-Ying Zheng
- Department of Cardiology, First Affiliated Hospital of Xinjiang Medical University, Urumqi, China
| | - Fen Liu
- Department of Cardiology, First Affiliated Hospital of Xinjiang Medical University, Urumqi, China
| | - Yi-Ning Yang
- Department of Cardiology, First Affiliated Hospital of Xinjiang Medical University, Urumqi, China
| | - Xiao-Mei Li
- Department of Cardiology, First Affiliated Hospital of Xinjiang Medical University, Urumqi, China
| | - Xiang Ma
- Department of Cardiology, First Affiliated Hospital of Xinjiang Medical University, Urumqi, China
| | - Yi-Tong Ma
- Department of Cardiology, First Affiliated Hospital of Xinjiang Medical University, Urumqi, China
| | - Xiang Xie
- Department of Cardiology, First Affiliated Hospital of Xinjiang Medical University, Urumqi, China
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Michalski B, Szymczyk E, Peczek L, Nawrot B, Kupczynska K, Krzemińska-Pakuła M, Peruga JZ, Lipiec P, Kasprzak JD. The role of selected adipokines and ghrelin in the prognosis after myocardial infarction in a 12-month follow-up in the presence of metabolic syndrome. Arch Med Sci 2017; 13:785-794. [PMID: 28721146 PMCID: PMC5510508 DOI: 10.5114/aoms.2017.65659] [Citation(s) in RCA: 9] [Impact Index Per Article: 1.1] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 06/14/2016] [Accepted: 09/26/2016] [Indexed: 11/17/2022] Open
Abstract
INTRODUCTION The aim of this study was to evaluate the predictive value of selected adipokines in the improvement in the ejection fraction and in the development of adverse cardiac remodeling during 12 months of follow-up among patients with an ST-segment elevation acute myocardial infarction (STEMI) in the presence of metabolic syndrome (MeS). MATERIAL AND METHODS The study population consisted of 69 patients (49 male; mean age: 59 ±10 years) with a first STEMI that was treated with a primary percutaneous coronary intervention (pPCI). In this group, 36 patients (18 male; mean age: 60 ±15 years) had MeS according to the definition of the International Diabetes Federation. The baseline clinical evaluation included a clinical examination and evaluation of the blood levels of C-reactive protein, ghrelin, resistin, and fasting glucose. Within 72 h after the STEMI, an echocardiographic examination was performed. A complete clinical evaluation was repeated after 12 months. Adverse cardiac remodeling was defined as an increase in the left ventricular end-diastolic volume of ≥ 8%. An improvement of the ejection fraction (EF) was defined as an increase of more than 5% in the EF. RESULTS A concentration of ghrelin ≤ 160.46 pg/ml (AUC = 0.71, p = 0.032) had a good predictive value for the occurrence of adverse left ventricular remodeling but only in the patients without MeS. Among the patients with MeS, a concentration of resistin ≤ 5196 pg/ml (AUC = 0.073, p = 0.024) had a good predictive value for the occurrence of left ventricular remodeling. A concentration of leptin > 52.18 pg/ml (AUC = 0.81, p < 0.0001) and resistin > 4419.27 ng/ml (AUC = 0.67, p = 0.049) had a good predictive value for improvement of the LVEF in the patients without MeS. CONCLUSIONS The selected adipokines had a good predictive value for the development of adverse cardiac remodeling and for improvement of the ejection fraction among patients after a STEMI in the presence of metabolic syndrome.
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Affiliation(s)
- Błażej Michalski
- Department of Cardiology, Medical University of Lodz, Lodz, Poland
| | - Ewa Szymczyk
- Department of Cardiology, Medical University of Lodz, Lodz, Poland
| | - Lukasz Peczek
- Department of Bioorganic Chemistry, Centre of Molecular and Macromolecular Studies of the Polish Academy of Sciences, Lodz, Poland
| | - Barbara Nawrot
- Department of Bioorganic Chemistry, Centre of Molecular and Macromolecular Studies of the Polish Academy of Sciences, Lodz, Poland
| | | | | | - Jan Z. Peruga
- Department of Cardiology, Medical University of Lodz, Lodz, Poland
| | - Piotr Lipiec
- Department of Cardiology, Medical University of Lodz, Lodz, Poland
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Fuster JJ, Ouchi N, Gokce N, Walsh K. Obesity-Induced Changes in Adipose Tissue Microenvironment and Their Impact on Cardiovascular Disease. Circ Res 2017; 118:1786-807. [PMID: 27230642 DOI: 10.1161/circresaha.115.306885] [Citation(s) in RCA: 452] [Impact Index Per Article: 56.5] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Grants] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 11/13/2015] [Accepted: 02/16/2016] [Indexed: 02/07/2023]
Abstract
Obesity is causally linked with the development of cardiovascular disorders. Accumulating evidence indicates that cardiovascular disease is the collateral damage of obesity-driven adipose tissue dysfunction that promotes a chronic inflammatory state within the organism. Adipose tissues secrete bioactive substances, referred to as adipokines, which largely function as modulators of inflammation. The microenvironment of adipose tissue will affect the adipokine secretome, having actions on remote tissues. Obesity typically leads to the upregulation of proinflammatory adipokines and the downregulation of anti-inflammatory adipokines, thereby contributing to the pathogenesis of cardiovascular diseases. In this review, we focus on the microenvironment of adipose tissue and how it influences cardiovascular disorders, including atherosclerosis and ischemic heart diseases, through the systemic actions of adipokines.
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Affiliation(s)
- José J Fuster
- From the Whitaker Cardiovascular Institute, Boston University School of Medicine, Boston, MA (J.J.F., N.G., K.W.); and Department of Molecular Cardiology, Nagoya University School of Medicine, Nagoya, Japan (N.O.).
| | - Noriyuki Ouchi
- From the Whitaker Cardiovascular Institute, Boston University School of Medicine, Boston, MA (J.J.F., N.G., K.W.); and Department of Molecular Cardiology, Nagoya University School of Medicine, Nagoya, Japan (N.O.)
| | - Noyan Gokce
- From the Whitaker Cardiovascular Institute, Boston University School of Medicine, Boston, MA (J.J.F., N.G., K.W.); and Department of Molecular Cardiology, Nagoya University School of Medicine, Nagoya, Japan (N.O.)
| | - Kenneth Walsh
- From the Whitaker Cardiovascular Institute, Boston University School of Medicine, Boston, MA (J.J.F., N.G., K.W.); and Department of Molecular Cardiology, Nagoya University School of Medicine, Nagoya, Japan (N.O.).
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21
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Buturak A, Değirmencioğlu A, Bayrak F, Kırış T, Karakurt H, Demir AR, Sürgit Ö, Ertürk M. Elective percutaneous coronary intervention leads to significant changes in serum resistin, leptin, and adiponectin levels regardless of periprocedural myocardial injury: an observational study. Anatol J Cardiol 2016; 16:940-946. [PMID: 27443475 PMCID: PMC5324914 DOI: 10.14744/anatoljcardiol.2016.6876] [Citation(s) in RCA: 3] [Impact Index Per Article: 0.3] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Download PDF] [Journal Information] [Subscribe] [Scholar Register] [Accepted: 03/14/2016] [Indexed: 12/26/2022] Open
Abstract
OBJECTIVE Bioactive roles of adipokines in coronary atherosclerosis and acute coronary syndromes have been demonstrated previously. However, there is a lack of data regarding the relationship between serum adipokines and periprocedural myocardial injury (PMI) following elective percutaneous coronary intervention (PCI). Therefore, we aimed to investigate the association between serum adipokines and PMI related to elective PCI. METHODS In total, 153 consecutive patients (aged 60.6±8.2 years, 98 men) with stable angina pectoris undergoing elective PCI were enrolled in this observational cross-sectional study. Serum resistin, leptin, adiponectin, and high-sensitive Troponin T (hscTnT) levels were measured immediately before PCI and after 12-h PCI. The no-injury, PMI, and type 4a myocardial infarction (type 4a MI) groups were defined as groups consisting patients with post-procedural hscTnT concentrations <14 ng/L, between 14-70 ng/L, and >70 ng/L, respectively. RESULTS Serum hscTnT, resistin, and leptin concentrations significantly (p<0.001) increased while serum adiponectin levels decreased (p<0.001) after 12-h elective PCI. However, no correlation was found between post-procedural hscTnT concentrations and resistin, leptin, and adiponectin levels. The no-injury group consisted of 65 patients (42.4%), whereas PMI and type 4a MI were observed in 70 (45.8%) and 18 (11.8%) patients, respectively. The average pre-procedural and post-procedural resistin, leptin, and adiponectin levels did not show any significant difference in the no-injury, PMI, and type 4a MI groups. CONCLUSION There is no correlation between serum adipokine levels and post-procedural troponin elevations reflecting PMI or type 4a MI. However, serum resistin and leptin levels increase, whereas adiponectin levels decrease significantly after elective PCI.
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Affiliation(s)
- Ali Buturak
- Department of Cardiology, Faculty of Medicine, Acıbadem University; İstanbul-Turkey.
| | - Aleks Değirmencioğlu
- Department of Cardiology, Faculty of Medicine, Acıbadem University; İstanbul-Turkey
| | - Fatih Bayrak
- Department of Cardiology, Faculty of Medicine, Acıbadem University; İstanbul-Turkey
| | - Tuncay Kırış
- Department of Cardiology, Katip Çelebi University Atatürk Research Hospital; İzmir-Turkey
| | - Hüseyin Karakurt
- Department of Cardiology, Mehmet Akif Ersoy Cardiovascular Surgery Education and Research Hospital; İstanbul-Turkey
| | - Ali Rıza Demir
- Department of Cardiology, Mehmet Akif Ersoy Cardiovascular Surgery Education and Research Hospital; İstanbul-Turkey
| | - Özgür Sürgit
- Department of Cardiology, Mehmet Akif Ersoy Cardiovascular Surgery Education and Research Hospital; İstanbul-Turkey
| | - Mehmet Ertürk
- Department of Cardiology, Mehmet Akif Ersoy Cardiovascular Surgery Education and Research Hospital; İstanbul-Turkey
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Joksić J, Sopić M, Spasojević-Kalimanovska V, Gojković T, Zeljković A, Vekić J, Andjelkovic K, Kalimanovska-Oštrić D, Jelić-Ivanović Z. Higher circulating resistin protein and PBMCs resistin mRNA levels are associated with increased prevalence of small dense LDL particles in coronary artery disease patients. Clin Exp Pharmacol Physiol 2015; 43:22-8. [DOI: 10.1111/1440-1681.12503] [Citation(s) in RCA: 7] [Impact Index Per Article: 0.7] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 07/30/2015] [Revised: 10/08/2015] [Accepted: 10/09/2015] [Indexed: 11/28/2022]
Affiliation(s)
- Jelena Joksić
- Department of Medical Biochemistry; Faculty of Pharmacy; Belgrade Serbia
| | - Miron Sopić
- Department of Medical Biochemistry; Faculty of Pharmacy; Belgrade Serbia
| | | | - Tamara Gojković
- Department of Medical Biochemistry; Faculty of Pharmacy; Belgrade Serbia
| | | | - Jelena Vekić
- Department of Medical Biochemistry; Faculty of Pharmacy; Belgrade Serbia
| | - Kristina Andjelkovic
- Institute for Cardiovascular Diseases; Clinical Center of Serbia; Belgrade Serbia
| | - Dimitra Kalimanovska-Oštrić
- Institute for Cardiovascular Diseases; Clinical Center of Serbia; Belgrade Serbia
- School of Medicine University of Belgrade; Belgrade Serbia
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On-Statin Resistin, Leptin, and Risk of Recurrent Coronary Events After Hospitalization for an Acute Coronary Syndrome (from the Pravastatin or Atorvastatin Evaluation and Infection Therapy-Thrombolysis in Myocardial Infarction 22 Study). Am J Cardiol 2015; 116:694-8. [PMID: 26119654 DOI: 10.1016/j.amjcard.2015.05.038] [Citation(s) in RCA: 15] [Impact Index Per Article: 1.5] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 04/22/2015] [Revised: 05/28/2015] [Accepted: 05/28/2015] [Indexed: 11/20/2022]
Abstract
Resistin is an adipokine secreted by macrophages and inflammatory cells linked to insulin resistance and inflammation. Leptin is an adipokine regulator of appetite and obesity. Although circulating levels of both have been associated with atherosclerosis, few data have reported their relation to coronary events in the context of statin therapy. This study measured on-statin levels of both resistin and leptin through enzyme-linked immunosorbent assay in a nested case-control cohort (n = 176 cases with coronary death, myocardial infarction, or unstable angina pectoris observed in follow-up matched 1:1 to 176 controls) derived from the Pravastatin or Atorvastatin Evaluation and Infection Therapy-Thrombolysis in Myocardial Infarction 22 study, a randomized controlled trial of atorvastatin 80 mg/day versus pravastatin 40 mg/day in patients with a recent acute coronary syndrome. Resistin demonstrated a moderate association with high-sensitivity C-reactive protein (hsCRP; Spearman rho = 0.25, p <0.0001). On-statin resistin levels were linked to recurrent coronary events in conditional logistic regression analysis adjusted for additional risk factors including hsCRP and history of diabetes (tertile 3 vs 1 adjusted odds ratio 2.08; 95% confidence interval [CI] 1.04 to 4.19). An additive risk was noted when patients were stratified by resistin and glycated hemoglobin levels. In contrast, leptin levels were associated with obesity, diabetes, triglycerides, and hsCRP (p <0.001 for each) but demonstrated no association with recurrent coronary events (tertile 3 vs 1 adjusted odds ratio 0.72; 95% CI 0.28 to 1.83). In conclusion, on-statin resistin, but not leptin, is an independent marker of residual risk for recurrent coronary events in patients after hospitalization for an acute coronary syndrome.
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Abstract
There is evidence that patients with moderate to severe psoriasis have an increased risk of conditions such as cardiovascular disease, obesity, diabetes mellitus, and metabolic syndrome. The precise mechanisms underlying the observed increase in cardiovascular disease in psoriasis remain to be defined but inflammatory pathways mutual to both conditions are probably involved. Suppression of systemic inflammation in psoriasis could help reduce cardiovascular inflammation but robust evidence is still lacking evidence is lacking. This article summarizes the current literature on cardiovascular and metabolic comorbidities in psoriasis, identifies research gaps, and suggests management strategies to reduce cardiovascular risk in patients with moderate to severe psoriasis.
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25
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Maresca F, Di Palma V, Bevilacqua M, Uccello G, Taglialatela V, Giaquinto A, Esposito G, Trimarco B, Cirillo P. Adipokines, vascular wall, and cardiovascular disease: a focused overview of the role of adipokines in the pathophysiology of cardiovascular disease. Angiology 2015; 66:8-24. [PMID: 24535638 DOI: 10.1177/0003319713520463] [Citation(s) in RCA: 21] [Impact Index Per Article: 2.1] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 08/29/2023]
Abstract
Epidemiological evidence has shown that abdominal obesity is closely associated with the development of cardiovascular (CV) disease, suggesting that it might be considered as an independent CV risk factor. However, the pathophysiological mechanisms responsible for the association between these 2 clinical entities remain largely unknown. Adipocytes are considered able to produce and secrete chemical mediators known as "adipokines" that may exert several biological actions, including those on heart and vessels. Of interest, a different adipokine profile can be observed in the plasma of patients with obesity or metabolic syndrome compared with healthy controls. We consider the main adipokines, focusing on their effects on the vascular wall and analyzing their role in CV pathophysiology.
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Affiliation(s)
- Fabio Maresca
- Department of Advanced Biomedical Sciences, Division of Cardiology, University of Naples, Naples, Italy
| | - Vito Di Palma
- Department of Advanced Biomedical Sciences, Division of Cardiology, University of Naples, Naples, Italy
| | - Michele Bevilacqua
- Department of Advanced Biomedical Sciences, Division of Cardiology, University of Naples, Naples, Italy
| | - Giuseppe Uccello
- Department of Advanced Biomedical Sciences, Division of Cardiology, University of Naples, Naples, Italy
| | - Vittorio Taglialatela
- Department of Advanced Biomedical Sciences, Division of Cardiology, University of Naples, Naples, Italy
| | - Alessandro Giaquinto
- Department of Advanced Biomedical Sciences, Division of Cardiology, University of Naples, Naples, Italy
| | - Giovanni Esposito
- Department of Advanced Biomedical Sciences, Division of Cardiology, University of Naples, Naples, Italy
| | - Bruno Trimarco
- Department of Advanced Biomedical Sciences, Division of Cardiology, University of Naples, Naples, Italy
| | - Plinio Cirillo
- Department of Advanced Biomedical Sciences, Division of Cardiology, University of Naples, Naples, Italy
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Singh P, Sridhar MG, Rajappa M, Balachander J, Kadhiravan T. Adiponectin-resistin index and its strong association with acute coronary syndrome in South Indian men. Inflamm Res 2014; 63:961-8. [PMID: 25217005 DOI: 10.1007/s00011-014-0771-z] [Citation(s) in RCA: 4] [Impact Index Per Article: 0.4] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 02/13/2014] [Revised: 08/08/2014] [Accepted: 09/03/2014] [Indexed: 10/24/2022] Open
Abstract
BACKGROUND India has the highest burden of acute coronary syndromes worldwide. Apart from certain lipid alterations that have been established to be definite risk factors, low level of adiponectin, high levels of resistin, and IL-6 have been shown to be risk factors for cardiovascular events. Insulin resistance is also a significant predictor of poor outcome in patients admitted with ACS. METHODS 69 male patients with ACS and 70 age-matched healthy males were recruited in the study. Insulin, total adiponectin, resistin, and IL-6 levels were assayed in all study subjects. Indices of insulin resistance and novel adipokine indices were calculated using standard formulae. Multiple logistic regression analysis was done to find out the best predictor of ACS. RESULTS Resistin, IL-6, insulin resistance indices, AR index, and IRAR index were found to be significantly higher, while insulin sensitivity indices and total adiponectin were found to be lower in cases, as compared with controls (p < 0.001). Insulin resistance was found to be higher in the admission sample, when compared to the fasting sample in patients with ACS (p = 0.01). On multivariate logistic regression analysis, HOMA-IR and AR index were found to be significantly associated with ACS. AR index was the best independent predictor of ACS, with the highest odds ratio (AR index: adjusted OR 17.528, p < 0.0001 versus HOMA-IR: adjusted OR 1.146, p = 0.001). CONCLUSIONS The present results implicate that adipokines are significantly associated with pathogenesis of ACS, warranting adequate and early appropriate treatment to reverse this metabolic dysregulation. In our study, AR index was the best predictor of ACS. Hence, the novel AR index might be useful in routine clinical practice for screening persons with increased risk of future development of ACS.
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Affiliation(s)
- Prerna Singh
- Department of Biochemistry, Jawaharlal Institute of Postgraduate Medical Education and Research (JIPMER), Puducherry, 605006, India
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Chedraui P, Pérez-López FR, Escobar GS, Palla G, Montt-Guevara M, Cecchi E, Genazzani AR, Simoncini T. Circulating leptin, resistin, adiponectin, visfatin, adipsin and ghrelin levels and insulin resistance in postmenopausal women with and without the metabolic syndrome. Maturitas 2014; 79:86-90. [PMID: 25015014 DOI: 10.1016/j.maturitas.2014.06.008] [Citation(s) in RCA: 63] [Impact Index Per Article: 5.7] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 04/24/2014] [Revised: 06/02/2014] [Accepted: 06/10/2014] [Indexed: 12/13/2022]
Abstract
OBJECTIVE To measure serum levels of adipsin, leptin, resistin, adiponectin, visfatin, ghrelin and insulin in postmenopausal women screened for the metabolic syndrome (METS). METHODS Serum of 100 postmenopausal women was analyzed using multiplex technology for the mentioned analytes. In addition, values for the homeostasis model assessment of insulin resistance (HOMA-IR) were calculated. Comparisons were performed in accordance to the presence or not of the METS and each of its components. Criteria of the American Heart Association were used to define the METS. RESULTS Age and time since menopause onset were similar in women with the METS (n=57) as compared to those without the syndrome (n=43). METS women displayed significantly higher levels of adipsin, leptin, resistin, insulin and HOMA-IR values and lower adiponectin levels. These differences were mainly observed among women with abdominal obesity, independent of fulfilling METS criteria or not. In this same sense, lower adiponectin levels significantly related to low HDL-C and high triglyceride levels; and higher insulin and HOMA-IR values related to high triglyceride and glucose levels, respectively. CONCLUSION In this sample, postmenopausal women with the METS displayed higher insulin and adipokine levels. These were mainly related to abdominal obesity and metabolic and lipid abnormalities. More research is warranted in this regard.
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Affiliation(s)
- Peter Chedraui
- Institute of Biomedicine, Research Area for Women's Health, Facultad de Ciencias Médicas, Universidad Católica de Santiago de Guayaquil, Guayaquil, Ecuador.
| | - Faustino R Pérez-López
- Department of Obstetrics and Gynecology, Facultad de Medicina, Lozano Blesa University Hospital, Universidad de Zaragoza, Zaragoza, Spain
| | - Gustavo S Escobar
- Institute of Biomedicine, Research Area for Women's Health, Facultad de Ciencias Médicas, Universidad Católica de Santiago de Guayaquil, Guayaquil, Ecuador
| | - Giulia Palla
- Department of Clinical and Experimental Medicine, Division of Obstetrics and Gynecology, University of Pisa, Pisa, Italy
| | - Magdalena Montt-Guevara
- Department of Clinical and Experimental Medicine, Division of Obstetrics and Gynecology, University of Pisa, Pisa, Italy
| | - Elena Cecchi
- Department of Clinical and Experimental Medicine, Division of Obstetrics and Gynecology, University of Pisa, Pisa, Italy
| | - Andrea R Genazzani
- Department of Clinical and Experimental Medicine, Division of Obstetrics and Gynecology, University of Pisa, Pisa, Italy
| | - Tommaso Simoncini
- Department of Clinical and Experimental Medicine, Division of Obstetrics and Gynecology, University of Pisa, Pisa, Italy
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Obesity and Psoriasis: Inflammatory Nature of Obesity, Relationship Between Psoriasis and Obesity, and Therapeutic Implications. ACTAS DERMO-SIFILIOGRAFICAS 2014. [DOI: 10.1016/j.adengl.2012.08.024] [Citation(s) in RCA: 6] [Impact Index Per Article: 0.5] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 12/17/2022] Open
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Cabrera de León A, Almeida González D, González Hernández A, Juan Alemán Sánchez J, Brito Díaz B, Domínguez Coello S, Marcelino Rodríguez I, Gregorio Oliva García J, Aguirre Jaime A, Rodríguez Pérez MDC. The association of resistin with coronary disease in the general population. J Atheroscler Thromb 2013; 21:273-81. [PMID: 24201007 DOI: 10.5551/jat.19273] [Citation(s) in RCA: 13] [Impact Index Per Article: 1.1] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 12/29/2022] Open
Abstract
AIMS To explore the association between resistin expression and the incidence of ischemic heart disease in the general population. METHODS A follow-up study of 6636 adults recruited randomly from the general population. RESULTS The serum resistin concentration was higher in women (6.1 ng/mL; CI95%=6.0-6.2) than in men (5.6 ng/mL; CI95%=5.5-5.7). Individuals in the 5th quintile or higher of resistin (RQ5) were younger (P＜0.001) and had a lower prevalence of arterial hypertension (P＜0.001), abdominal obesity (P＜0.001), diabetes (P＜0.001) and dyslipidemia (P＜0.001). The cardiovascular risk estimated by the Framingham function was also lower in the RQ5 subgroup (P＜0.001); however, the prevalence of smoking was higher (P＜0.001), as was the prevalence of low HDL cholesterol (P＜0.001). After 3.5 years of follow-up, the RQ5 subgroup had a higher incidence of acute myocardial infarction (AMI, RR=1.9; CI95%=1.01-3.54). In the population without diabetes, the RQ5 subgroup had a higher risk of AMI (RR=2.4; CI95%=1.10-5.17), and the risk of AMI was highest in women in this group (4.97; CI95%=1.33-18.57). The risk levels were significant in the Cox models adjusted for age, sex and smoking; and the hazard ratio was 2.5 for AMI (CI95%=1.29-4.70) in the sample of patients matched by sex and smoking status. CONCLUSIONS Resistin may be a risk marker for ischemic heart disease in the general population. The serum resistin concentration is higher in women, and the associated increase in the risk of AMI based on the resistin level is also higher in women than in men.
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Atwa M, Emara A, Balata M, Youssef N, Bayoumy N, Sherif A, Fiala L. Serum leptin, adiponectin, and resistin among adult patients with acanthosis nigricans: correlations with insulin resistance and risk factors for cardiovascular disease. Int J Dermatol 2013; 53:e410-20. [DOI: 10.1111/ijd.12340] [Citation(s) in RCA: 9] [Impact Index Per Article: 0.8] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 11/30/2022]
Affiliation(s)
- Mona Atwa
- Department of Dermatology and Venereology; Suez Canal University; Ismailia Egypt
| | - Amany Emara
- Department of Clinical Pathology; Ain Shams University; Cairo Egypt
| | - Mona Balata
- Department of Physical Medicine, Rheumatology and Rehabilitation; Ain Shams University; Cairo Egypt
| | - Nahed Youssef
- Department of Clinical Pathology; Suez Canal University; Ismailia Egypt
| | - Nervana Bayoumy
- Department of Physiology; College of Medicine; King Saud University; Riyadh Saudi Arabia
| | | | - Lamia Fiala
- Department of Community and Occupational Medicine; Suez Canal University; Ismailia Egypt
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Baldasseroni S, Mannucci E, Di Serio C, Orso F, Bartoli N, Mossello E, Foschini A, Monami M, Valoti P, Fumagalli S, Colombi C, Pellerito S, Gensini G, Marchionni N, Tarantini F. Resistin level in coronary artery disease and heart failure: the central role of kidney function. J Cardiovasc Med (Hagerstown) 2013; 14:150-7. [PMID: 22240747 DOI: 10.2459/jcm.0b013e32834eec93] [Citation(s) in RCA: 10] [Impact Index Per Article: 0.8] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 12/17/2022]
Abstract
OBJECTIVES The aim of this study was to evaluate resistin levels in patients with coronary artery disease (CAD) with or without chronic heart failure, in order to define its independent predictor. METHODS One hundred and seven outpatients with CAD were enrolled in the study and divided into three groups: CAD without left-ventricular systolic dysfunction (group 1); CAD with left-ventricular dysfunction without heart failure symptoms (group 2); CAD with overt heart failure (group 3). Plasma resistin was determined by ELISA. RESULTS Resistin progressively increased from group 1 (10.7±5.0 ng/ml) to groups 2 (11.8±5.8 ng/ml) and 3 (17.0±6.8 ng/ml), with the difference reaching statistical significance in group 3 versus groups 1 and 2 (P=0.001). A multivariable model of analysis demonstrated that the best predictor of plasma resistin level was the estimated glomerular filtration rate (P<0.001), indicating that reduction of kidney function was the main cause of the adipokine increase observed in patients with CAD and overt heart failure. CONCLUSIONS Our data confirm the rise of resistin plasma levels previously described in patients affected by chronic heart failure; however, in our study, this relationship seemed to be mediated mainly by the level of kidney function, and only partially by the severity of ventricular dysfunction.
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Affiliation(s)
- Samuele Baldasseroni
- Department of Critical Care Medicine and Surgery, University of Florence and Azienda Ospedaliero-Universitaria Careggi, Viale Morgagni 85, Florence, Italy.
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Carrascosa JM, Rocamora V, Fernandez-Torres RM, Jimenez-Puya R, Moreno JC, Coll-Puigserver N, Fonseca E. Obesity and psoriasis: inflammatory nature of obesity, relationship between psoriasis and obesity, and therapeutic implications. ACTAS DERMO-SIFILIOGRAFICAS 2012. [PMID: 23177976 DOI: 10.1016/j.ad.2012.08.003] [Citation(s) in RCA: 88] [Impact Index Per Article: 6.8] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 12/13/2022] Open
Abstract
Obesity, particularly abdominal obesity, is currently considered a chronic low-grade inflammatory condition that plays an active role in the development of the pathophysiologic phenomena responsible for metabolic syndrome and cardiovascular disease through the secretion of proinflammatory adipokines and cytokines. In recent years clear genetic, pathogenic, and epidemiologic links have been established between psoriasis and obesity, with important implications for health. The relationship between the 2 conditions is probably bidirectional, with obesity predisposing to psoriasis and psoriasis favoring obesity. Obesity also has important implications in the treatment of psoriasis, such as a greater risk of adverse effects with conventional systemic drugs and reduced efficacy and/or increased cost with biologic agents, for which dosage should be adjusted to the patient's weight.
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Affiliation(s)
- J M Carrascosa
- Servicio de Dermatología, Hospital Universitari Germans Trias i Pujol, Badalona, Barcelona, España.
| | - V Rocamora
- Servicio de Dermatología, Hospital de Manacor, Manacor, Mallorca, España
| | | | - R Jimenez-Puya
- Servicio de Dermatología, Hospital Universitario Reina Sofía, Madrid, España
| | - J C Moreno
- Servicio de Dermatología, Hospital Universitario Reina Sofía, Madrid, España
| | - N Coll-Puigserver
- Servicio de Dermatología, Hospital de Manacor, Manacor, Mallorca, España
| | - E Fonseca
- Complejo Hospitalario Universitario de La Coruña, La Coruña, España
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Elshishtawy H, Ibrahim SE, Helmi A, Farouk N, Elshinnawy MA. Resistin in systemic lupus erythematosus: Relation to lupus nephritis and premature atherosclerosis. EGYPTIAN RHEUMATOLOGIST 2012. [DOI: 10.1016/j.ejr.2012.06.001] [Citation(s) in RCA: 19] [Impact Index Per Article: 1.5] [Reference Citation Analysis] [Track Full Text] [Subscribe] [Scholar Register] [Indexed: 01/24/2023]
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Abstract
An adipokine, resistin, was discovered as a potential mediator of obesity related insulin resistance in rodents. However, the relevance of resistin in human obesity and insulin resistance has been challenged by the difference between human and rodent resistin and the controversies in human epidemiologic studies. Instead, recent human clinical studies and experiments support the idea that human resistin is an inflammatory mediator and a biomarker of cardiovascular diseases, especially in atherosclerosis and heart failure. Thus, we focused on the recent evidence of the role of human resistin in cardiovascular disease.
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Affiliation(s)
- Sang Eun Lee
- National Research Laboratory for Cardiovascular Stem Cell Niche, Korea
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Abstract
Resistin has been implicated in coronary atherosclerotic disease and congestive heart failure. Recent studies have extended its involvement in peripheral artery disease. Despite some controversial data, the mainstream clinical literature supports that resistin is associated with both coronary and peripheral artery diseases including ischemic stroke. In this review, the multiple roles of resistin as screening, diagnostic, and prognostic marker for cardiovascular disease are discussed. The independence of resistin in disease prediction and diagnosis appears complicated by its confounders, such as C-reactive protein. A clear-cut biomarker function of resistin in cardiovascular disease needs be clarified by additional large-scale, well-designed prospective studies.
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Affiliation(s)
- Qinxue Ding
- Division of Vascular and Endovascular Surgery, Department of Surgery, Stanford University, Stanford, CA 94350, USA
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Northcott JM, Yeganeh A, Taylor CG, Zahradka P, Wigle JT. Adipokines and the cardiovascular system: mechanisms mediating health and disease. Can J Physiol Pharmacol 2012; 90:1029-59. [DOI: 10.1139/y2012-053] [Citation(s) in RCA: 52] [Impact Index Per Article: 4.0] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 12/15/2022]
Abstract
This review focuses on the role of adipokines in the maintenance of a healthy cardiovascular system, and the mechanisms by which these factors mediate the development of cardiovascular disease in obesity. Adipocytes are the major cell type comprising the adipose tissue. These cells secrete numerous factors, termed adipokines, into the blood, including adiponectin, leptin, resistin, chemerin, omentin, vaspin, and visfatin. Adipose tissue is a highly vascularised endocrine organ, and different adipose depots have distinct adipokine secretion profiles, which are altered with obesity. The ability of many adipokines to stimulate angiogenesis is crucial for adipose tissue expansion; however, excessive blood vessel growth is deleterious. As well, some adipokines induce inflammation, which promotes cardiovascular disease progression. We discuss how these 7 aforementioned adipokines act upon the various cardiovascular cell types (endothelial progenitor cells, endothelial cells, vascular smooth muscle cells, pericytes, cardiomyocytes, and cardiac fibroblasts), the direct effects of these actions, and their overall impact on the cardiovascular system. These were chosen, as these adipokines are secreted predominantly from adipocytes and have known effects on cardiovascular cells.
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Affiliation(s)
- Josette M. Northcott
- Department of Biochemistry and Medical Genetics, University of Manitoba, Winnipeg, MB R3E OJ9, Canada
- Institute of Cardiovascular Sciences, and Medicine, St. Boniface Hospital Research Centre, Winnipeg, MB R2H 2A6, Canada
| | - Azadeh Yeganeh
- Department of Physiology, University of Manitoba, Winnipeg, MB R3E OJ9, Canada
- Canadian Centre for Agri-Food Research in Health and Medicine, St. Boniface Hospital Research Centre, Winnipeg, MB R3T 2N2, Canada
| | - Carla G. Taylor
- Department of Physiology, University of Manitoba, Winnipeg, MB R3E OJ9, Canada
- Department of Human Nutritional Sciences, University of Manitoba, Winnipeg, MB R3E OJ9, Canada
- Canadian Centre for Agri-Food Research in Health and Medicine, St. Boniface Hospital Research Centre, Winnipeg, MB R3T 2N2, Canada
| | - Peter Zahradka
- Department of Physiology, University of Manitoba, Winnipeg, MB R3E OJ9, Canada
- Department of Human Nutritional Sciences, University of Manitoba, Winnipeg, MB R3E OJ9, Canada
- Canadian Centre for Agri-Food Research in Health and Medicine, St. Boniface Hospital Research Centre, Winnipeg, MB R3T 2N2, Canada
| | - Jeffrey T. Wigle
- Department of Biochemistry and Medical Genetics, University of Manitoba, Winnipeg, MB R3E OJ9, Canada
- Institute of Cardiovascular Sciences, and Medicine, St. Boniface Hospital Research Centre, Winnipeg, MB R2H 2A6, Canada
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Role of adipokines in atherosclerosis: interferences with cardiovascular complications in rheumatic diseases. Mediators Inflamm 2012; 2012:125458. [PMID: 22910888 PMCID: PMC3403095 DOI: 10.1155/2012/125458] [Citation(s) in RCA: 51] [Impact Index Per Article: 3.9] [Reference Citation Analysis] [Abstract] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 06/06/2012] [Accepted: 06/19/2012] [Indexed: 01/08/2023] Open
Abstract
Patients with rheumatic diseases have an increased risk of mortality by cardiovascular events. In fact, several rheumatic diseases such as rheumatoid arthritis, osteoarthritis, systemic lupus erythematosus, and ankylosing spondylitis are associated with a higher prevalence of cardiovascular diseases (CVDs). Although traditional cardiovascular risk factors have been involved in the pathogenesis of cardiovascular diseases in rheumatic patients, these alterations do not completely explain the enhanced cardiovascular risk in this population. Obesity and its pathologic alteration of fat mass and dysfunction, due to an altered pattern of secretion of proinflammatory adipokines, could be one of the links between cardiovascular and rheumatic diseases. Indeed, the incidence of CVDs is augmented in obese individuals with rheumatic disorders. Thus, in this paper we explore in detail the relationships among adipokines, rheumatic diseases, and cardiovascular complications by giving to the reader a holistic vision and several suggestions for future perspectives and potential clinical implications.
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Jamaluddin MS, Weakley SM, Yao Q, Chen C. Resistin: functional roles and therapeutic considerations for cardiovascular disease. Br J Pharmacol 2012. [PMID: 21545576 DOI: 10.1111/j.1476-5381.2011] [Citation(s) in RCA: 3] [Impact Index Per Article: 0.2] [Reference Citation Analysis] [Abstract] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 01/01/2023] Open
Abstract
UNLABELLED Resistin, originally described as an adipocyte-specific hormone, has been suggested to be an important link between obesity, insulin resistance and diabetes. Although its expression was initially defined in adipocytes, significant levels of resistin expression in humans are mainly found in mononuclear leukocytes, macrophages, spleen and bone marrow cells. Increasing evidence indicates that resistin plays important regulatory roles apart from its role in insulin resistance and diabetes in a variety of biological processes: atherosclerosis and cardiovascular disease (CVD), non-alcoholic fatty liver disease, autoimmune disease, malignancy, asthma, inflammatory bowel disease and chronic kidney disease. As CVD accounts for a significant amount of morbidity and mortality in patients with diabetes and without diabetes, it is important to understand the role that adipokines such as resistin play in the cardiovascular system. Evidence suggests that resistin is involved in pathological processes leading to CVD including inflammation, endothelial dysfunction, thrombosis, angiogenesis and smooth muscle cell dysfunction. The modes of action and signalling pathways whereby resistin interacts with its target cells are beginning to be understood. In this review, the current knowledge about the functions and pathophysiological implications of resistin in CVD development is summarized; clinical translations, therapeutic considerations and future directions in the field of resistin research are discussed. LINKED ARTICLES This article is part of a themed section on Fat and Vascular Responsiveness. To view the other articles in this section visit http://dx.doi.org/10.1111/bph.2012.165.issue-3.
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Affiliation(s)
- Md S Jamaluddin
- Molecular Surgeon Research Center, Division of Vascular Surgery and Endovascular Therapy, Michael E. DeBakey Department of Surgery, Baylor College of Medicine, Houston, TX 77030, USA
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Jamaluddin MS, Weakley SM, Yao Q, Chen C. Resistin: functional roles and therapeutic considerations for cardiovascular disease. Br J Pharmacol 2012; 165:622-32. [PMID: 21545576 DOI: 10.1111/j.1476-5381.2011.01369.x] [Citation(s) in RCA: 339] [Impact Index Per Article: 26.1] [Reference Citation Analysis] [Abstract] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 12/17/2022] Open
Abstract
UNLABELLED Resistin, originally described as an adipocyte-specific hormone, has been suggested to be an important link between obesity, insulin resistance and diabetes. Although its expression was initially defined in adipocytes, significant levels of resistin expression in humans are mainly found in mononuclear leukocytes, macrophages, spleen and bone marrow cells. Increasing evidence indicates that resistin plays important regulatory roles apart from its role in insulin resistance and diabetes in a variety of biological processes: atherosclerosis and cardiovascular disease (CVD), non-alcoholic fatty liver disease, autoimmune disease, malignancy, asthma, inflammatory bowel disease and chronic kidney disease. As CVD accounts for a significant amount of morbidity and mortality in patients with diabetes and without diabetes, it is important to understand the role that adipokines such as resistin play in the cardiovascular system. Evidence suggests that resistin is involved in pathological processes leading to CVD including inflammation, endothelial dysfunction, thrombosis, angiogenesis and smooth muscle cell dysfunction. The modes of action and signalling pathways whereby resistin interacts with its target cells are beginning to be understood. In this review, the current knowledge about the functions and pathophysiological implications of resistin in CVD development is summarized; clinical translations, therapeutic considerations and future directions in the field of resistin research are discussed. LINKED ARTICLES This article is part of a themed section on Fat and Vascular Responsiveness. To view the other articles in this section visit http://dx.doi.org/10.1111/bph.2012.165.issue-3.
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Affiliation(s)
- Md S Jamaluddin
- Molecular Surgeon Research Center, Division of Vascular Surgery and Endovascular Therapy, Michael E. DeBakey Department of Surgery, Baylor College of Medicine, Houston, TX 77030, USA
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Ibrahim HH, Korah TE, Badr EA, Elshafie MK. Serum resistin in acute myocardial infarction patients with and without diabetes mellitus. Egypt Heart J 2012. [DOI: 10.1016/j.ehj.2011.08.036] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 10/16/2022] Open
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Cirillo P, Maresca F, Di Palma V, Ziviello F, Bevilacqua M. Adipose tissue in the pathophysiology of cardiovascular disease: Who is guilty? World J Hypertens 2012; 2:13. [DOI: 10.5494/wjh.v2.i1.13] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Track Full Text] [Download PDF] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 02/06/2023] Open
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Schwartz DR, Lazar MA. Human resistin: found in translation from mouse to man. Trends Endocrinol Metab 2011; 22:259-65. [PMID: 21497511 PMCID: PMC3130099 DOI: 10.1016/j.tem.2011.03.005] [Citation(s) in RCA: 137] [Impact Index Per Article: 9.8] [Reference Citation Analysis] [Abstract] [MESH Headings] [Grants] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 01/20/2011] [Revised: 02/26/2011] [Accepted: 03/15/2011] [Indexed: 12/28/2022]
Abstract
The discovery of resistin 10 years ago as a fat cell-secreted factor that modulates insulin resistance suggested a link to the current obesity-associated epidemics of diabetes and cardiovascular disease, which are major human health concerns. Although adipocyte-derived resistin is indisputably linked to insulin resistance in rodent models, the relevance of human resistin is complicated because human resistin is secreted by macrophages rather than adipocytes, and because of the descriptive nature of human epidemiology. In this review, we examine the recent and growing evidence that human resistin is an inflammatory biomarker and a potential mediator of diabetes and cardiovascular disease.
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Abstract
Adipose tissue is an active endocrine organ contributing to the regulation of multiple metabolic pathways via self-produced bioactive products called adipokines. These adipokines are key players in the pathogenesis of metabolic syndrome and cardiovascular diseases. Co-occurrence of obesity and psoriasis could lead to interactions of both diseases in which adipokines, at least in part, are involved and may contribute to associated comorbidities of psoriasis. Until today numerous adipokines have been identified of which the most important ones are discussed in the following within the context of obesity, chronic inflammation and their possible role in the pathogenesis of psoriasis. Adipokines could serve as a missing link in the causal relationship between psoriasis and comorbidities and may provide a biomarker for disease severity, risk of comorbidities and treatment success.
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Affiliation(s)
- Sascha Gerdes
- Psoriasis-Center at the Department of Dermatology, University Medical Center Schleswig-Holstein, Campus Kiel, Kiel, Germany.
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Koç F, Tokaç M, Kocabaş V, Kaya C, Büyükbaş S, Erdem S, Karabağ T, Demir K, Alihanoğlu Y, Kaya A. Ghrelin, Resistin and Leptin Levels in
Patients with Metabolic Syndrome. ELECTRONIC JOURNAL OF GENERAL MEDICINE 2011. [DOI: 10.29333/ejgm/82707] [Citation(s) in RCA: 3] [Impact Index Per Article: 0.2] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 11/21/2022]
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El-Barbary AM, Hussein MS, Rageh EM, Hamouda HE, Wagih AA, Ismail RG. Effect of atorvastatin on inflammation and modification of vascular risk factors in rheumatoid arthritis. J Rheumatol 2010; 38:229-35. [PMID: 21041278 DOI: 10.3899/jrheum.100582] [Citation(s) in RCA: 60] [Impact Index Per Article: 4.0] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 11/22/2022]
Abstract
OBJECTIVE To investigate the effect of atorvastatin therapy on inflammation, disease activity, endothelial dysfunction, and arterial stiffness in patients with rheumatoid arthritis (RA). METHODS This study included 30 patients with early RA, randomly divided into 2 groups. Group 1 (n = 15) received methotrexate (MTX; 0.2 mg/kg/week; mean (15.5 ± SD 1.3) plus prednisone (10 mg/day). Group 2 (n = 15) received MTX and prednisone with the same previous doses plus atorvastatin therapy (40 mg/day). Ten healthy individuals of similar age and sex served as controls. Disease activity, lipid profile, serum malondialdehyde (MDA), tumor necrosis factor-α (TNF-α), resistin, adiponectin, and brachial artery flow-mediated dilation (FMD) were measured before and after 6 months of treatment. RESULTS Atorvastatin combined with MTX therapy significantly reduced serum total cholesterol, low-density lipoprotein cholesterol, and triglycerides, and increased high-density lipoprotein cholesterol (p < 0.001). Disease activity variables, serum MDA, TNF-α, resistin, adiponectin, and FMD were significantly improved by the drug combinations (p < 0.001). CONCLUSION Atorvastatin therapy in patients with RA reduced disease activity and conventional and novel vascular risk factors that promote the atheromatous lesion. Therapy was also associated with concomitant improvement in endothelial function.
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Affiliation(s)
- Amal M El-Barbary
- Department of Rheumatology and Rehabilitation, Tanta Faculty of Medicine, Elgesh Street, Egyt Tanta, 002 Egypt.
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Usefulness of assessing circulating levels of resistin, ghrelin, and IL-18 in alcoholic acute pancreatitis. Dig Dis Sci 2010; 55:2982-7. [PMID: 20108040 DOI: 10.1007/s10620-009-1106-8] [Citation(s) in RCA: 19] [Impact Index Per Article: 1.3] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 08/17/2009] [Accepted: 12/10/2009] [Indexed: 12/22/2022]
Abstract
OBJECTIVES Acute pancreatitis (AP) is a severe inflammatory disease with high mortality and morbidity rates. We have previously demonstrated that resistin may represent an early marker of inflammation in AP. It was also revealed that ghrelin may have anti-inflammatory potential. However, the role of adipohormones in AP-resistin and ghrelin as well as the proinflammatory cytokine interleukin (IL)-18-has not yet been fully elucidated. METHODS The study group comprised 32 patients with alcoholic AP and 30 controls matched for age, sex, and body mass index (BMI). In all cases AP was classified as grade C according to Balthazar's computed tomography (CT) score and as severe (3 points) according to Ranson's criteria. Serum levels of resistin, ghrelin, and IL-18 were measured on first, third, and fifth day of hospitalization by enzyme-linked immunosorbent assay (ELISA). RESULTS On first day of hospitalization the mean serum resistin concentration in AP patients was significantly higher than in controls (P < 0.05) and further increased on third and fifth day of hospitalization (17.4 ± 4.23 ng/ml and 25.8 ± 8.14 ng/ml, respectively). On first day of hospitalization the mean serum IL-18 concentration in AP patients was significantly higher than in controls (P < 0.05), on third day its level further increased, and on fifth day it decreased to a level similar to that observed on admission. The serum ghrelin concentrations on first, third, and fifth day of hospitalization were comparable, and significantly higher than in controls (P < 0.01). Significant correlation between C-reactive protein (CRP) and resistin levels (r = 0.43; P < 0.05) and between CRP and IL-18 (r = 0.58; P <0.05) on day of admission was found. CONCLUSIONS Serum concentration of IL-18 and resistin may contribute to inflammatory response and may be useful as an early marker of inflammation in AP. We also suspect that ghrelin affects the course of AP and plays an important role in inflammatory response.
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Chen C, Jiang J, Lü JM, Chai H, Wang X, Lin PH, Yao Q. Resistin decreases expression of endothelial nitric oxide synthase through oxidative stress in human coronary artery endothelial cells. Am J Physiol Heart Circ Physiol 2010; 299:H193-201. [PMID: 20435848 DOI: 10.1152/ajpheart.00431.2009] [Citation(s) in RCA: 158] [Impact Index Per Article: 10.5] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 12/25/2022]
Abstract
Resistin is a newly discovered adipocyte-derived cytokine that may play an important role in insulin resistance, diabetes, adipogenesis, inflammation, and cardiovascular disease. However, it is largely unknown whether resistin impairs endothelial functions by affecting the endothelial nitric oxide synthase (eNOS) system. In this study, we determined the effect of human recombinant resistin protein on eNOS expression and regulation in human coronary artery endothelial cells (HCAECs). When cells were treated with clinically relevant concentrations of resistin (40 or 80 ng/ml) for 24 h, the levels of eNOS mRNA, protein, and activity and eNOS mRNA stability were significantly reduced. Cellular nitric oxide levels were also decreased. In addition, the cellular levels of reactive oxygen species (ROS), including superoxide anion, were significantly increased in resistin-treated HCAECs. Mitochondrial membrane potential and the activities of catalase and superoxide dismutase were reduced. Three antioxidants, seleno-L-methionine, ginsenoside Rb1, and MnTBAP (superoxide dismutase mimetic), effectively blocked resistin-induced eNOS downregulation. Meanwhile, resistin activated the mitogen-activated protein kinases p38 and c-Jun NH(2)-terminal kinase (JNK), and the specific p38 inhibitor SB-239063 effectively blocked resistin-induced ROS production and eNOS downregulation. Furthermore, immunoreactivity of resistin was increased in atherosclerotic regions of human aorta and carotid arteries. Thus resistin directly induces eNOS downregulation through overproduction of ROS and activation of p38 and JNK in HCAECs. Resistin-induced mitochondrial dysfunction and imbalance in cellular redox enzymes may be the underlying mechanisms of oxidative stress.
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Affiliation(s)
- Changyi Chen
- Division of Vascular Surgery and Endovascular Therapy, Michael E. DeBakey Dept. of Surgery, Baylor College of Medicine, One Baylor Plaza, Houston, TX 77030, USA.
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Hussain S, Asghar M, Javed Q. Resistin gene promoter region polymorphism and the risk of hypertrophic cardiomyopathy in patients. Transl Res 2010; 155:142-7. [PMID: 20171599 DOI: 10.1016/j.trsl.2009.10.002] [Citation(s) in RCA: 17] [Impact Index Per Article: 1.1] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 06/09/2009] [Revised: 10/08/2009] [Accepted: 10/12/2009] [Indexed: 10/20/2022]
Abstract
Resistin, a novel cytokine, is associated with an inflammatory process and is suggested to induce hypertrophy in rat cardiomyocytes. Resistin gene expression has not been investigated in patients with hypertrophic cardiomyopathy (HCM). This study investigates resistin levels in HCM patients and healthy controls and the molecular basis for the regulation of the resistin gene (RETN) in a Pakistani population. Patients with HCM (n = 105) and healthy individuals (n = 110) were enrolled in this investigation. Serum resistin levels were determined by enzyme-linked immunosorbent assay (ELISA). RETN genotyping was performed by polymerase chain reaction (PCR) and DNA sequencing. Our data showed a statistically significant increase in resistin levels from HCM patients compared with healthy subjects (6.3 +/- 2.7 ng/mL in patients vs 3.4 +/- 2.1 ng/mL in controls, P < 0.0001). The RETN -420 C > G polymorphism was significantly high in patients with HCM compared with the control group (P < 0.001). There was a significant difference between the C and G alleles from HCM cases and controls (odds ratio [OR] = 3.54, 95% confidence interval [CI] = 2.36-5.30, P < 0.0001). Logistic-regression analysis showed that the increased resistin levels, and the RETN-420 C > G polymorphism were significantly associated with HCM. Our data suggest that the elevated resistin levels and the RETN -420 C > G polymorphism may be associated with cardiac hypertrophy in the study population.
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Affiliation(s)
- Sabir Hussain
- Department of Biochemistry, Quaid-i-Azam University, Islamabad 45320, Pakistan
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Lee DH, Jeon HK, Park HJ, Shin WS, Lee SW, Youn HJ, Kim CM, Lee HK. Change in ischemia-modified albumin and its clinical significance during exercise stress testing. Circ J 2010; 74:484-9. [PMID: 20057159 DOI: 10.1253/circj.cj-09-0581] [Citation(s) in RCA: 7] [Impact Index Per Article: 0.5] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 11/09/2022]
Abstract
BACKGROUND There is little data about the additive effects of ischemia-modified albumin (IMA) on the exercise stress test (EST) used for the screening of ischemic heart disease. The relationship between myocardial ischemic burden and the change in IMA (DeltaIMA) during EST was investigated. METHODS AND RESULTS EST was performed using the Bruce protocol to evaluate chest pain or exertional dyspnea in 155 patients (men 89, 53+/-13 years). Blood samples for IMA were obtained before and immediately after EST. According to the EST results and the pattern of DeltaIMA, patients were categorized into 3 groups (none was classified as EST(-)/DeltaIMA(+)): (1) (EST(-); (2) EST(+)/DeltaIMA(-); and (3) EST(+)/DeltaIMA(+). After EST, 60 of 155 (38.7%) patients were EST(+) and 14/60 (23.3%) were EST(+)/DeltaIMA(+). Duke treadmill score was significantly lower in the EST(+)/DeltaIMA(+) group compared with the other groups (-9.0+/-7.9, -1.7+/-4.2, 6.7+/-4.4, respectively, P<0.001); 43/60 (72%) patients with EST(+) underwent coronary angiography and the proportion of patients with a large ischemic burden was higher in the EST(+)/DeltaIMA(+)group compared with the EST(+)/DeltaIMA(-) group (72.7% vs 15.6%, P=0.001). CONCLUSIONS Increased IMA after EST suggests a large ischemic burden in coronary artery disease, so the DeltaIMA during EST may be useful for predicting the severity of myocardial ischemia.
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Affiliation(s)
- Dong-Hyeon Lee
- Division of Cardiology, Department of Internal Medicine, The Catholic University of Medical College, Uijongbu city, Kyungki-do, Republic of Korea
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Wang H, Chen DY, Cao J, He ZY, Zhu BP, Long M. High serum resistin level may be an indicator of the severity of coronary disease in acute coronary syndrome. ACTA ACUST UNITED AC 2009; 24:161-6. [PMID: 19848317 DOI: 10.1016/s1001-9294(09)60082-1] [Citation(s) in RCA: 35] [Impact Index Per Article: 2.2] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 01/28/2023]
Abstract
OBJECTIVE To investigate the correlation between serum resistin level, cardiovascular risk factors and severity of coronary disease in acute coronary syndrome (ACS). METHODS After evaluated by clinical history, electrocardiography, exercise tolerance tests, laboratory tests, and coronary angiography, 220 consecutive patients with suspected chest pain were divided into normal control group, stable angina pectoris (SAP) group, and ACS group, respectively. Baseline clinical characteristics, including height, weight, waist circumference, hip circumference, white blood cell count, high-sensitive C-reactive protein (hsCRP), total cholesterol, triglyceride, low-density lipoprotein cholesterol and high-density lipoprotein cholesterol, were compared among three groups. ELISA was used to detect serum resistin levels. Pearson's correlation coefficient analysis was used to assess association between resistin and other traditional cardiovascular risk factors. Multinomial logistic regression analyses were used to define the relationship between serum resistin level and SAP or ACS. RESULTS Serum resistin level in ACS group (1.18+/-0.48 microg/L) was significantly higher than that in normal control and SAP groups (0.49+/-0.40 and 0.66+/-0.40 microg/L; P<0.01). Only in ACS group, increased serum resistin level was significantly correlated with hsCRP (r=0.262, P=0.004) and white blood cell count (r=0.347, P=0.001). Furthermore, serum resistin levels showed a stepwise increase with the number increase of > 50% stenosed coronary vessels. Multinomial logistic regression test demonstrated that serum resistin was a strong risk factor for ACS (OR=29.132, 95 % CI: 10.939-77.581, P<0.001). CONCLUSION These findings suggested the potential role of resistin in atherosclerosis and especially its involvement in ACS.
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Affiliation(s)
- Hao Wang
- Department of Geriatric Cardiology, Chinese People's Liberation Army General Hospital, Beijing 100853, China
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