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Kim MJ, Kim SW, Ha B, Kim HS, Kwon SH, Jin J, Choi YK, Park KG, Kim JG, Lee IK, Jeon JH. Persistent influence of past obesity on current adiponectin levels and mortality in patients with type 2 diabetes. Korean J Intern Med 2025; 40:299-309. [PMID: 40102712 PMCID: PMC11938665 DOI: 10.3904/kjim.2024.221] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Grants] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 06/22/2024] [Revised: 10/04/2024] [Accepted: 10/28/2024] [Indexed: 03/20/2025] Open
Abstract
BACKGROUND/AIMS Adiponectin, a hormone primarily produced by adipocytes, typically shows an inverse relationship with body mass index (BMI). However, some studies have reported a positive correlation between the two. Thus, this study aimed to examine the relationship between adiponectin level and BMI in diabetic patients, focusing on the impact of past obesity on current adiponectin levels. METHODS We conducted an observational study analyzing data from 323 diabetic patients at Kyungpook National University Hospital. Based on past and current BMIs, participants were categorized into never-obese (nn, n = 106), previously obese (on, n = 43), and persistently obese (oo, n = 73) groups based on a BMI threshold of 25 kg/m2. Adiponectin level and BMI were key variables. Kaplan-Meier analysis assessed their impact on all-cause mortality up to August 2023, with survival differences based on adiponectin quartiles and follow-up starting from patient enrollment (2010-2015). RESULTS The analysis revealed a significant inverse correlation between adiponectin level and past maximum BMI. The on group exhibited approximately 10% lower adiponectin levels compared to the nn group. This association remained significant after adjusting for current BMI, age, and sex, highlighting the lasting influence of previous obesity on adiponectin levels. Furthermore, survival analysis indicated that patients in the lowest adiponectin quartile had reduced survival, with a statistically significant trend (p = 0.062). CONCLUSION Findings of this study suggest that lower adiponectin levels, potentially reflecting past obesity, are associated with decreased survival in diabetic patients, underscoring a critical role of adiponectin in long-term health outcomes.
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Affiliation(s)
- Min-Ji Kim
- Department of Internal Medicine, Kyungpook National University Chilgok Hospital, School of Medicine, Kyungpook National University, Daegu,
Korea
| | - Sung-Woo Kim
- Department of Internal Medicine, Daegu Catholic University Hospital, Daegu Catholic University School of Medicine, Daegu,
Korea
| | - Bitna Ha
- Department of Internal Medicine, Kyungpook National University Hospital, School of Medicine, Kyungpook National University, Daegu,
Korea
| | - Hyang Sook Kim
- Department of Internal Medicine, Kyungpook National University Hospital, School of Medicine, Kyungpook National University, Daegu,
Korea
| | - So-Hee Kwon
- Department of Internal Medicine, Kyungpook National University Chilgok Hospital, School of Medicine, Kyungpook National University, Daegu,
Korea
| | - Jonghwa Jin
- Department of Internal Medicine, Kyungpook National University Hospital, School of Medicine, Kyungpook National University, Daegu,
Korea
| | - Yeon-Kyung Choi
- Department of Internal Medicine, Kyungpook National University Chilgok Hospital, School of Medicine, Kyungpook National University, Daegu,
Korea
| | - Keun-Gyu Park
- Department of Internal Medicine, Kyungpook National University Hospital, School of Medicine, Kyungpook National University, Daegu,
Korea
| | - Jung Guk Kim
- Department of Internal Medicine, Kyungpook National University Hospital, School of Medicine, Kyungpook National University, Daegu,
Korea
| | - In-Kyu Lee
- Department of Internal Medicine, Kyungpook National University Hospital, School of Medicine, Kyungpook National University, Daegu,
Korea
| | - Jae-Han Jeon
- Department of Internal Medicine, Kyungpook National University Chilgok Hospital, School of Medicine, Kyungpook National University, Daegu,
Korea
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Shi H, Sim YJ. Effects of weekend-focused exercise on obesity-related hormones and metabolic syndrome markers in male high school students. J Exerc Rehabil 2024; 20:227-234. [PMID: 39781501 PMCID: PMC11704708 DOI: 10.12965/jer.2448632.316] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Journal Information] [Subscribe] [Scholar Register] [Received: 10/29/2024] [Revised: 11/21/2024] [Accepted: 11/24/2024] [Indexed: 01/12/2025] Open
Abstract
To examine the changes in obesity-related hormones and metabolic syndrome markers in male high school students with obesity following a weekend-focused moderate- or high-intensity exercise program at the recommended weekly physical activity level, or a program of regular exercise 3 times a week at moderate intensity, over a 10-week period. Forty-eight male high school students who were obese with a body fat percentage of ≥25% were randomly assigned to one of three groups: a regular moderate-intensity exercise group (n=17) that freely selected and performed moderate-intensity aerobic and resistance training exercises, every Monday, Wednesday, and Friday, for a total of 150-300 min/wk; a weekend-focused moderate-intensity exercise group (n=15) that freely selected and performed aerobic and resistance training exercises every Saturday for 150-300 min; and a week-end-focused high-intensity exercise group (n=16) that freely selected and performed aerobic and resistance training exercises every Sunday for 75-150 min. Insulin and leptin levels significantly decreased in all the groups, with the greatest reduction in the regular exercise group. Abdominal circumference and triglyceride levels significantly decreased in all the groups. Fasting glucose decreased only in the regular exercise group. High-density lipoprotein cholesterol significantly increased in both the regular and weekend-focused moderate-intensity exercise groups. No significant differences in adiponectin levels, and systolic and diastolic blood pressure were observed between the groups. A weekend-focused exercise program has health effects similar to those of regular exercise, highlighting the importance of meeting the recommended weekly physical activity levels.
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Affiliation(s)
- Haoyu Shi
- Department of Physical Education, Kunsan National University, Gunsan,
Korea
| | - Young-Je Sim
- Department of Physical Education, Kunsan National University, Gunsan,
Korea
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Ko JKY, Li HWR, Lam KSL, Tam S, Lee VCY, Yeung TWY, Ho PC, Ng EHY. Serum adiponectin is independently associated with the metabolic syndrome in Hong Kong, Chinese women with polycystic ovary syndrome. Gynecol Endocrinol 2016; 32:390-4. [PMID: 26699091 DOI: 10.3109/09513590.2015.1126708] [Citation(s) in RCA: 12] [Impact Index Per Article: 1.3] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 01/15/2023] Open
Abstract
OBJECTIVE To evaluate the association of serum adiponectin level with the metabolic syndrome in Chinese women with polycystic ovary syndrome (PCOS). METHODS This was a cross-sectional study carried out in Hong Kong Chinese women with PCOS at a university-affiliated tertiary hospital between January 2010 and January 2011. Clinical and biochemical parameters of the women were analysed. Prediction of the metabolic syndrome was determined by receiver-operator characteristic (ROC) curves, univariate and multivariate logistic regression analyses. RESULTS A total of 116 women diagnosed to have PCOS were analysed. The area under the ROC curve of adiponectin for the prediction of metabolic syndrome was 0.820, 95% confidence interval (CI) 0.737-0.886. Univariate binary logistic regression showed that testosterone, sex hormone-binding globulin (SHBG), free androgen index (FAI), waist circumference, body mass index (BMI), quantitative insulin-sensitivity check index (QUICKI), homeostasis model assessment of insulin resistance (HOMA-IR) and adiponectin were significantly associated with the metabolic syndrome. On multivariate logistic regression analysis, adiponectin (p = 0.020), HOMA-IR, age (p = 0.011) and BMI (p = 0.019) were independently associated with the metabolic syndrome, but not FAI (p = 0.256). CONCLUSIONS Serum adiponectin is independently associated with the metabolic syndrome in Chinese women with PCOS. Further longitudinal follow-up studies are needed to determine whether serum adiponectin adds to the prediction of long-term cardiometabolic morbidity conferred by age, BMI and measures of insulin resistance.
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Affiliation(s)
- Jennifer Ka Yee Ko
- a Department of Obstetrics and Gynaecology , The University of Hong Kong, Queen Mary Hospital , Hong Kong
| | - Hang Wun Raymond Li
- a Department of Obstetrics and Gynaecology , The University of Hong Kong, Queen Mary Hospital , Hong Kong
| | - Karen Siu Ling Lam
- b Department of Medicine , The University of Hong Kong, Queen Mary Hospital , Hong Kong , and
| | - Sidney Tam
- b Department of Medicine , The University of Hong Kong, Queen Mary Hospital , Hong Kong , and
- c Department of Pathology and Clinical Biochemistry , The University of Hong Kong, Queen Mary Hospital , Hong Kong
| | - Vivian Chi Yan Lee
- a Department of Obstetrics and Gynaecology , The University of Hong Kong, Queen Mary Hospital , Hong Kong
| | - Tracy Wing Yee Yeung
- a Department of Obstetrics and Gynaecology , The University of Hong Kong, Queen Mary Hospital , Hong Kong
| | - Pak Chung Ho
- a Department of Obstetrics and Gynaecology , The University of Hong Kong, Queen Mary Hospital , Hong Kong
| | - Ernest Hung Yu Ng
- a Department of Obstetrics and Gynaecology , The University of Hong Kong, Queen Mary Hospital , Hong Kong
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Kawwass JF, Summer R, Kallen CB. Direct effects of leptin and adiponectin on peripheral reproductive tissues: a critical review. Mol Hum Reprod 2015; 21:617-632. [PMID: 25964237 PMCID: PMC4518135 DOI: 10.1093/molehr/gav025] [Citation(s) in RCA: 51] [Impact Index Per Article: 5.1] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Grants] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 01/14/2015] [Revised: 04/22/2015] [Accepted: 05/05/2015] [Indexed: 08/13/2023] Open
Abstract
Obesity is a risk factor for infertility and adverse reproductive outcomes. Adipose tissue is an important endocrine gland that secretes a host of endocrine factors, called adipokines, which modulate diverse physiologic processes including appetite, metabolism, cardiovascular function, immunity and reproduction. Altered adipokine expression in obese individuals has been implicated in the pathogenesis of a host of health disorders including diabetes and cardiovascular disease. It remains unclear whether adipokines play a significant role in the pathogenesis of adverse reproductive outcomes in obese individuals and, if so, whether the adipokines are acting directly or indirectly on the peripheral reproductive tissues. Many groups have demonstrated that receptors for the adipokines leptin and adiponectin are expressed in peripheral reproductive tissues and that these adipokines are likely, therefore, to exert direct effects on these tissues. Many groups have tested for direct effects of leptin and adiponectin on reproductive tissues including the testis, ovary, uterus, placenta and egg/embryo. The hypothesis that decreased fertility potential or adverse reproductive outcomes may result, at least in part, from defects in adipokine signaling within reproductive tissues has also been tested. Here, we present a critical analysis of published studies with respect to two adipokines, leptin and adiponectin, for which significant data have been generated. Our evaluation reveals significant inconsistencies and methodological limitations regarding the direct effects of these adipokines on peripheral reproductive tissues. We also observe a pervasive failure to account for in vivo data that challenge observations made in vitro. Overall, while leptin and adiponectin may directly modulate peripheral reproductive tissues, existing data suggest that these effects are minor and non-essential to human or mouse reproductive function. Current evidence suggests that direct effects of leptin or adiponectin on peripheral reproductive tissues are unlikely to factor significantly in the adverse reproductive outcomes observed in obese individuals.
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Affiliation(s)
- Jennifer F Kawwass
- Department of Gynecology and Obstetrics, Division of Reproductive Endocrinology and Infertility, Emory University School of Medicine, 1639 Pierce Drive, WMB 4217, Atlanta, GA 30322, USA
| | - Ross Summer
- Center for Translational Medicine, Thomas Jefferson University, 1020 Walnut Street, Philadelphia, PA 19107, USA
| | - Caleb B Kallen
- Division of Reproductive Endocrinology and Infertility, Department of Obstetrics and Gynecology, Thomas Jefferson University, 833 Chestnut Street, Suite C-152, Philadelphia, PA 19107, USA
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Ayer J, Charakida M, Deanfield JE, Celermajer DS. Lifetime risk: childhood obesity and cardiovascular risk. Eur Heart J 2015; 36:1371-6. [PMID: 25810456 DOI: 10.1093/eurheartj/ehv089] [Citation(s) in RCA: 123] [Impact Index Per Article: 12.3] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 12/22/2014] [Accepted: 03/09/2015] [Indexed: 02/06/2023] Open
Abstract
In a recent report, the worldwide prevalence of childhood obesity was estimated to have increased by 47% between 1980 and 2013. As a result, substantial concerns have been raised about the future burden of cardiovascular (CV) disease that could ensue. The purpose of this review is to summarize and interpret (i) the evidence linking early life obesity with adverse changes in CV structure and function in childhood, (ii) the lifetime risk for CV disease resulting from obesity in childhood, and (iii) the potential effects of lifestyle interventions in childhood to ameliorate these risks.
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Affiliation(s)
- Julian Ayer
- The Heart Centre for Children, The Children's Hospital at Westmead, Sydney, Australia Sydney Medical School, University of Sydney, Sydney, Australia
| | - Marietta Charakida
- Institute of Cardiovascular Sciences, University College London, London, UK
| | - John E Deanfield
- Institute of Cardiovascular Sciences, University College London, London, UK
| | - David S Celermajer
- The Heart Centre for Children, The Children's Hospital at Westmead, Sydney, Australia Sydney Medical School, University of Sydney, Sydney, Australia Royal Prince Alfred Hospital, Sydney, Australia
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Anil Kumar S, Hima Kumari P, Shravan Kumar G, Mohanalatha C, Kavi Kishor PB. Osmotin: a plant sentinel and a possible agonist of mammalian adiponectin. FRONTIERS IN PLANT SCIENCE 2015; 6:163. [PMID: 25852715 PMCID: PMC4360817 DOI: 10.3389/fpls.2015.00163] [Citation(s) in RCA: 61] [Impact Index Per Article: 6.1] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Subscribe] [Scholar Register] [Received: 06/10/2014] [Accepted: 03/01/2015] [Indexed: 05/18/2023]
Abstract
Osmotin is a stress responsive antifungal protein belonging to the pathogenesis-related (PR)-5 family that confers tolerance to both biotic and abiotic stresses in plants. Protective efforts of osmotin in plants range from high temperature to cold and salt to drought. It lyses the plasma membrane of the pathogens. It is widely distributed in fruits and vegetables. It is a differentially expressed and developmentally regulated protein that protects the cells from osmotic stress and invading pathogens as well, by structural or metabolic alterations. During stress conditions, osmotin helps in the accumulation of the osmolyte proline, which quenches reactive oxygen species and free radicals. Osmotin expression results in the accumulation of storage reserves and increases the shelf-life of fruits. It binds to a seven-transmembrane-domain receptor-like protein and induces programmed cell death in Saccharomyces cerevisiae through RAS2/cAMP signaling pathway. Adiponectin, produced in adipose tissues of mammals, is an insulin-sensitizing hormone. Strangely, osmotin acts like the mammalian hormone adiponectin in various in vitro and in vivo models. Adiponectin and osmotin, the two receptor binding proteins do not share sequence similarity at the amino acid level, but interestingly they have a similar structural and functional properties. In experimental mice, adiponectin inhibits endothelial cell proliferation and migration, primary tumor growth, and reduces atherosclerosis. This retrospective work examines the vital role of osmotin in plant defense and as a potential targeted therapeutic drug for humans.
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Affiliation(s)
- S. Anil Kumar
- Department of Genetics, Osmania University, HyderabadIndia
| | - P. Hima Kumari
- Department of Genetics, Osmania University, HyderabadIndia
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Ghoshal K, Bhattacharyya M. Adiponectin: Probe of the molecular paradigm associating diabetes and obesity. World J Diabetes 2015; 6:151-166. [PMID: 25685286 PMCID: PMC4317307 DOI: 10.4239/wjd.v6.i1.151] [Citation(s) in RCA: 79] [Impact Index Per Article: 7.9] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 08/28/2014] [Revised: 10/09/2014] [Accepted: 12/17/2014] [Indexed: 02/05/2023] Open
Abstract
Type 2 diabetes is an emerging health challenge all over the world as a result of urbanization, high prevalence of obesity, sedentary lifestyle and other stress related factors compounded with the genetic prevalence. The health consequences and economic burden of the obesity and related diabetes mellitus epidemic are enormous. Different signaling molecules secreted by adipocytes have been implicated in the development of obesity and associated insulin resistance in type 2 diabetes. Human adiponectin, a 244-amino acid collagen-like protein is solely secreted by adipocytes and acts as a hormone with anti-inflammatory and insulin-sensitizing properties. Adiponectin secretion, in contrast to secretion of other adipokines, is paradoxically decreased in obesity which may be attributable to inhibition of adiponectin gene transcription. There are several mechanisms through which adiponectin may decrease the risk of type 2 diabetes, including suppression of hepatic gluconeogenesis, stimulation of fatty acid oxidation in the liver, stimulation of fatty acid oxidation and glucose uptake in skeletal muscle, and stimulation of insulin secretion. To date, no systematic review has been conducted that evaluate the potential importance of adiponectin metabolism in insulin resistance. In this review attempt has been made to explore the relevance of adiponectin metabolism for the development of diabetes mellitus. This article also identifies this novel target for prospective therapeutic research aiming successful management of diabetes mellitus.
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Mondello P, Mian M, Aloisi C, Famà F, Mondello S, Pitini V. Cancer Cachexia Syndrome: Pathogenesis, Diagnosis, and New Therapeutic Options. Nutr Cancer 2014; 67:12-26. [DOI: 10.1080/01635581.2015.976318] [Citation(s) in RCA: 35] [Impact Index Per Article: 3.2] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 02/08/2023]
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9
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Thijssen E, van Caam A, van der Kraan PM. Obesity and osteoarthritis, more than just wear and tear: pivotal roles for inflamed adipose tissue and dyslipidaemia in obesity-induced osteoarthritis. Rheumatology (Oxford) 2014; 54:588-600. [PMID: 25504962 DOI: 10.1093/rheumatology/keu464] [Citation(s) in RCA: 238] [Impact Index Per Article: 21.6] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 01/20/2023] Open
Abstract
OA is a degenerative joint disease characterized by articular cartilage degradation, osteophyte formation, synovitis, and subchondral bone sclerosis. One of OAs main risk factors is obesity. To date, it is not fully understood how obesity results in OA. Historically, this link was ascribed to excessive joint loading as a result of increased body weight. However, the association between obesity and OA in non-weight-bearing joints suggests a more complex aetiology for obesity-induced OA. In the present review, the link between obesity and OA is discussed. First, the historical view of altered joint loading leading to wear and tear of the joint is addressed. Subsequently, the effects of a disturbed lipid metabolism, low-grade inflammation, and adipokines on joint tissues are discussed and linked to OA. Taken together, inflamed adipose tissue and dyslipidaemia play pivotal roles in obesity-induced OA. It becomes increasingly clear that the link between obesity and OA transcends excessive loading.
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Affiliation(s)
- Eva Thijssen
- Experimental Rheumatology, Radboud University Medical Center, Nijmegen, The Netherlands
| | - Arjan van Caam
- Experimental Rheumatology, Radboud University Medical Center, Nijmegen, The Netherlands
| | - Peter M van der Kraan
- Experimental Rheumatology, Radboud University Medical Center, Nijmegen, The Netherlands
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Electroacupuncture decreases the leukocyte infiltration to white adipose tissue and attenuates inflammatory response in high fat diet-induced obesity rats. EVIDENCE-BASED COMPLEMENTARY AND ALTERNATIVE MEDICINE 2014; 2014:473978. [PMID: 25202333 PMCID: PMC4150518 DOI: 10.1155/2014/473978] [Citation(s) in RCA: 23] [Impact Index Per Article: 2.1] [Reference Citation Analysis] [Abstract] [Track Full Text] [Download PDF] [Figures] [Subscribe] [Scholar Register] [Received: 04/05/2014] [Revised: 07/08/2014] [Accepted: 07/09/2014] [Indexed: 01/22/2023]
Abstract
Suppression of white adipose tissue inflammatory signaling may contribute to the pathogenesis of obesity-induced inflammatory response. However, the precise mechanism of efficacy of acupuncture related to adipose tissue remains poorly understood. In the present study we evaluated the anti-inflammatory activities of 10 Hz electroacupuncture (EA) which was applied at the acupoint Zusanli (ST36) for 20 min per day in high-fat diet- (HFD-) induced obesity model. Treatment lasted for one week. Obese rats treated with EA showed significantly reduced body weight compared with the rats in HFD group. EA decreased the number of F4/80 and CD11b-positive macrophages in epididymal adipose tissue. We found that 10 Hz EA given 7 days/week at ST36 acupoints significantly alleviated macrophage recruitment and then improved the obesity-associated factors of sterol regulatory element-binding protein-1 (SREBP-1) and target genes expression in rats with HFD. Adipose tissue inflammatory responses indicated by tumor necrosis factor-α (TNF-α), IL-6, monocyte chemotactic protein-1 (MCP-1), and CD68 mRNA expression were significantly reduced by EA in obese rats. Additionally, EA was found to significantly reduced serum levels of TNF-α, IL-6, and IL-1 in this model. These results indicated that EA improved adipose tissue inflammatory response in obese rats, at least partly, via attenuation of lipogenesis signaling.
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Kakinoki S, Sakai Y, Takemura T, Hanagata N, Fujisato T, Ishihara K, Yamaoka T. Gene chip/PCR-array analysis of tissue response to 2-methacryloyloxyethyl phosphorylcholine (MPC) polymer surfaces in a mouse subcutaneous transplantation system. JOURNAL OF BIOMATERIALS SCIENCE-POLYMER EDITION 2014; 25:1658-72. [DOI: 10.1080/09205063.2014.939917] [Citation(s) in RCA: 11] [Impact Index Per Article: 1.0] [Reference Citation Analysis] [Track Full Text] [Subscribe] [Scholar Register] [Indexed: 02/03/2023]
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12
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Bharti P, Katagiri S, Nitta H, Nagasawa T, Kobayashi H, Takeuchi Y, Izumiyama H, Uchimura I, Inoue S, Izumi Y. Periodontal treatment with topical antibiotics improves glycemic control in association with elevated serum adiponectin in patients with type 2 diabetes mellitus. Obes Res Clin Pract 2014; 7:e129-e138. [PMID: 24331774 DOI: 10.1016/j.orcp.2011.11.005] [Citation(s) in RCA: 35] [Impact Index Per Article: 3.2] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 08/30/2011] [Revised: 11/19/2011] [Accepted: 11/22/2011] [Indexed: 02/07/2023]
Abstract
OBJECTIVES Chronic inflammation of periodontitis aggravates glycemic control in type 2 diabetic patients through aggravation of insulin resistance. Increased or decreased release of various inflammatory mediators, such as high sensitivity C-reactive protein (hs-CRP), tumor necrosis factor (TNF)-α, interleukin (IL)-6 and adipokines, such as adiponectin, leptin, and resistin, are presumed to be responsible for developing and progressing insulin resistance. The purpose of this study was to examine the effects of periodontal treatment on glycemic control, serum inflammatory mediators and adipokines in type 2 diabetes patients with periodontitis. METHODS Twenty-one type 2 diabetic patients with periodontitis received periodontal treatment with topical antibiotics (intervention group) and 8 patients did not receive periodontal treatment (control group). Periodontal examination, including probing pocket depth (PPD) and bleeding on probing (BOP), and blood sampling were performed at baseline, 2 and 6 months after periodontal treatments. Glycated hemoglobin (HbA1c), hs-CRP, TNF-α, IL-6, adiponectin, leptin, and resistin were analyzed. RESULTS In the intervention group, improvements of PPD and BOP, decrease in HbA1c and elevation of serum adiponectin were observed, while in the control group, all parameters were not changed. Generalized linear model revealed that changes of serum adiponectin and TNF-α and change of BOP correlated significantly with the reduction of HbA1c at 6 months after periodontal treatments. CONCLUSION The results demonstrated that periodontal treatment improves periodontal status and glycemic control with elevation of serum adiponectin in type 2 diabetic patients. The results suggest that HbA1c is reduced by amelioration of insulin resistance due to elevated serum adiponectin after periodontal treatments.
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Affiliation(s)
- Pariksha Bharti
- Global Center of Excellence Program, International Research Center for Molecular Science in Tooth and Bone Diseases, Tokyo Medical and Dental University Graduate School, Tokyo, Japan
| | - Sayaka Katagiri
- Section of Periodontology, Department of Hard Tissue Engineering, Tokyo Medical and Dental University Graduate School, Tokyo, Japan.
| | - Hiroshi Nitta
- Section of Behavioral Dentistry, Department of Comprehensive Oral Health Care, Tokyo Medical and Dental University Graduate School, Tokyo, Japan
| | - Toshiyuki Nagasawa
- Section of Periodontology and Endodontology, Health Sciences University of Hokkaido, Sapporo, Japan
| | - Hiroaki Kobayashi
- Section of Periodontology, Department of Hard Tissue Engineering, Tokyo Medical and Dental University Graduate School, Tokyo, Japan
| | - Yasuo Takeuchi
- Section of Periodontology, Department of Hard Tissue Engineering, Tokyo Medical and Dental University Graduate School, Tokyo, Japan
| | - Hajime Izumiyama
- Tokyo Medical and Dental University Medical Hospital, Tokyo, Japan
| | - Isao Uchimura
- Department of Clinical and Molecular Endocrinology, Tokyo Medical and Dental University Graduate School, Tokyo, Japan
| | - Shuji Inoue
- Department of Clinical Nutrition, Faculty of Health Care, Kiryu University, Gunma, Japan
| | - Yuichi Izumi
- Global Center of Excellence Program, International Research Center for Molecular Science in Tooth and Bone Diseases, Tokyo Medical and Dental University Graduate School, Tokyo, Japan
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Abstract
In most species, endogenous circadian clocks regulate 24-h rhythms of behavior and physiology. Clock disruption has been associated with decreased cognitive performance and increased propensity to develop obesity, diabetes, and cancer. Many hormonal factors show robust diurnal secretion rhythms, some of which are involved in mediating clock output from the brain to peripheral tissues. In this review, we describe the mechanisms of clock-hormone interaction in mammals, the contribution of different tissue oscillators to hormonal regulation, and how changes in circadian timing impinge on endocrine signalling and downstream processes. We further summarize recent findings suggesting that hormonal signals may feed back on circadian regulation and how this crosstalk interferes with physiological and metabolic homeostasis.
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Affiliation(s)
- Anthony H Tsang
- Circadian Rhythms Group, Max Planck Institute for Biophysical Chemistry, Göttingen, Germany Chronophysiology Group, Medical Department I, University of Lübeck, Ratzeburger Allee 160, 23538 Lübeck, Germany School of Medicine, University of Queensland, Brisbane, Queensland, Australia
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Ozkok A, Kanbay A, Odabas AR, Covic A, Kanbay M. Obstructive sleep apnea syndrome and chronic kidney disease: a new cardiorenal risk factor. Clin Exp Hypertens 2014; 36:211-6. [DOI: 10.3109/10641963.2013.804546] [Citation(s) in RCA: 22] [Impact Index Per Article: 2.0] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 01/13/2023]
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Jiang YD, Chuang LM, Pei D, Lee YJ, Wei JN, Sung FC, Chang TJ. Genetic Variations in the Kir6.2 Subunit (KCNJ11) of Pancreatic ATP-Sensitive Potassium Channel Gene Are Associated with Insulin Response to Glucose Loading and Early Onset of Type 2 Diabetes in Childhood and Adolescence in Taiwan. Int J Endocrinol 2014; 2014:983016. [PMID: 25309595 PMCID: PMC4189766 DOI: 10.1155/2014/983016] [Citation(s) in RCA: 7] [Impact Index Per Article: 0.6] [Reference Citation Analysis] [Abstract] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 05/02/2014] [Accepted: 08/20/2014] [Indexed: 11/18/2022] Open
Abstract
To investigate the role of E23K polymorphism of the KCNJ11 gene on early onset of type 2 diabetes in school-aged children/adolescents in Taiwan, we recruited 38 subjects with type 2 diabetes (ages 18.6 ± 6.6 years; body mass index percentiles 83.3 ± 15.4) and 69 normal controls (ages 17.3 ± 3.8 years; body mass index percentiles 56.7 ± 29.0) from a national surveillance for childhood/adolescent diabetes in Taiwan. We searched for the E23K polymorphism of the KCNJ11 gene. We found that type 2 diabetic subjects had higher carrier rate of E23K polymorphism of KCNJ11 gene than control subjects (P = 0.044). After adjusting for age, gender, body mass index percentiles, and fasting plasma insulin, the E23K polymorphism contributed to an increased risk for type 2 diabetes (P = 0.047). K23-allele-containing genotypes conferring increased plasma insulin level during OGTT in normal subjects. However, the diabetic subjects with the K23-allele-containing genotypes had lower fasting plasma insulin levels after adjustment of age and BMI percentiles. In conclusion, the E23K variant of the KCNJ11 gene conferred higher susceptibility to type 2 diabetes in children/adolescents. Furthermore, in normal glucose-tolerant children/adolescents, K23 allele carriers had a higher insulin response to oral glucose loading.
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Affiliation(s)
- Yi-Der Jiang
- Department of Internal Medicine, National Taiwan University Hospital, 7 Chung-Shan South Road, Taipei 10002, Taiwan
| | - Lee-Ming Chuang
- Department of Internal Medicine, National Taiwan University Hospital, 7 Chung-Shan South Road, Taipei 10002, Taiwan
- Graduate Institute of Preventive Medicine, School of Public Health, National Taiwan University, Taipei 10002, Taiwan
| | - Dee Pei
- Division of Endocrinology and Metabolism, Department of Internal Medicine, Cardinal Tien Hospital, Xindian 23148, Taiwan
| | - Yann-Jinn Lee
- Department of Pediatrics, Mackay General Hospital, Taipei 10449, Taiwan
| | - Jun-Nan Wei
- Chia Nan University of Pharmacy and Science, Tainan 71710, Taiwan
| | - Fung-Chang Sung
- Institute of Environmental Health, College of Public Health, China Medical University, Taichung 40447, Taiwan
| | - Tien-Jyun Chang
- Department of Internal Medicine, National Taiwan University Hospital, 7 Chung-Shan South Road, Taipei 10002, Taiwan
- *Tien-Jyun Chang:
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Hsu YJ, Wang LC, Yang WS, Yang CM, Yang CH. Effects of fenofibrate on adiponectin expression in retinas of streptozotocin-induced diabetic rats. J Diabetes Res 2014; 2014:540326. [PMID: 25525608 PMCID: PMC4267464 DOI: 10.1155/2014/540326] [Citation(s) in RCA: 5] [Impact Index Per Article: 0.5] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 08/23/2014] [Revised: 11/10/2014] [Accepted: 11/10/2014] [Indexed: 12/16/2022] Open
Abstract
Adiponectin has been associated with increased risks of microvascular complications in diabetes; however, its role in the development of diabetic retinopathy (DR) is unknown. Fenofibrate is a lipid-lowering agent that has been shown to be capable of preventing DR progression. We investigated the expression of adiponectin and its receptors in DR and evaluated the effects of fenofibrate on their expression. The mRNA and protein levels of adiponectin and its receptors were elevated in retinas of streptozotocin-induced diabetic rats and were suppressed following fenofibrate treatment. Immunofluorescence staining demonstrated that adiponectin and adipoR1 were expressed in cells located within blood vessels, the retinal ganglion, and the inner nuclear layer. AdipoR1 was strongly expressed whereas adipoR2 was only weekly expressed in vascular endothelial cells. The in vitro experiments showed that adiponectin expression was induced by high glucose concentrations in RGC-5 and RAW264.7 cells and was suppressed following fenofibrate treatment. AdipoR1 and adipoR2 levels in RGC-5 cells were elevated in high glucose concentrations and suppressed by fenofibrate. Our results demonstrated that adiponectin may be a proinflammatory mediator in diabetic retinas and fenofibrate appears to modulate the expression of adiponectin and its receptors in diabetic retinas, effectively reducing DR progression.
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Affiliation(s)
- Ying-Jung Hsu
- Graduate Institute of Clinical Medicine, College of Medicine, National Taiwan University, Taipei 100, Taiwan
| | - Lu-Chun Wang
- Department of Ophthalmology, National Taiwan University Hospital, Taipei 100, Taiwan
| | - Wei-Shiung Yang
- Graduate Institute of Clinical Medicine, College of Medicine, National Taiwan University, Taipei 100, Taiwan
- Department of Internal Medicine, National Taiwan University Hospital, Taipei 100, Taiwan
| | - Chung-May Yang
- Department of Ophthalmology, National Taiwan University Hospital, Taipei 100, Taiwan
| | - Chang-Hao Yang
- Department of Ophthalmology, National Taiwan University Hospital, College of Medicine, National Taiwan University, No. 7 Chung-Shan South Road, Taipei 100, Taiwan
- *Chang-Hao Yang:
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Golbidi S, Laher I. Exercise induced adipokine changes and the metabolic syndrome. J Diabetes Res 2014; 2014:726861. [PMID: 24563869 PMCID: PMC3915640 DOI: 10.1155/2014/726861] [Citation(s) in RCA: 133] [Impact Index Per Article: 12.1] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 07/25/2013] [Accepted: 10/18/2013] [Indexed: 12/25/2022] Open
Abstract
The lack of adequate physical activity and obesity created a worldwide pandemic. Obesity is characterized by the deposition of adipose tissue in various parts of the body; it is now evident that adipose tissue also acts as an endocrine organ capable of secreting many cytokines that are though to be involved in the pathophysiology of obesity, insulin resistance, and metabolic syndrome. Adipokines, or adipose tissue-derived proteins, play a pivotal role in this scenario. Increased secretion of proinflammatory adipokines leads to a chronic inflammatory state that is accompanied by insulin resistance and glucose intolerance. Lifestyle change in terms of increased physical activity and exercise is the best nonpharmacological treatment for obesity since these can reduce insulin resistance, counteract the inflammatory state, and improve the lipid profile. There is growing evidence that exercise exerts its beneficial effects partly through alterations in the adipokine profile; that is, exercise increases secretion of anti-inflammatory adipokines and reduces proinflammatory cytokines. In this paper we briefly describe the pathophysiologic role of four important adipokines (adiponectin, leptin, TNF-α, and IL-6) in the metabolic syndrome and review some of the clinical trials that monitored these adipokines as a clinical outcome before and after exercise.
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Affiliation(s)
- Saeid Golbidi
- Department of Pharmacology and Therapeutics, Faculty of Medicine, University of British Columbia, Vancouver, BC, Canada V6T 1Z3
| | - Ismail Laher
- Department of Pharmacology and Therapeutics, Faculty of Medicine, University of British Columbia, Vancouver, BC, Canada V6T 1Z3
- *Ismail Laher:
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Richard C, Royer MM, Couture P, Cianflone K, Rezvani R, Desroches S, Lamarche B. Effect of the Mediterranean diet on plasma adipokine concentrations in men with metabolic syndrome. Metabolism 2013; 62:1803-10. [PMID: 23993420 DOI: 10.1016/j.metabol.2013.07.012] [Citation(s) in RCA: 28] [Impact Index Per Article: 2.3] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 01/17/2013] [Revised: 07/09/2013] [Accepted: 07/24/2013] [Indexed: 11/26/2022]
Abstract
OBJECTIVE While a Mediterranean dietary pattern (MedDiet) has been associated with favorable changes in several features of metabolic syndrome (MetS), its impact on plasma adipokine concentrations remains largely unknown. The objective of this study was to determine the impact of the MedDiet consumed under controlled feeding conditions, without (-WL) and with weight loss (+WL), on plasma adipokine concentrations in adult men with MetS (NCEP-ATP III). MATERIALS/METHODS The diet of 26 men with MetS (age 24 to 62 yrs) was first standardized to a North American control diet for 5 weeks. Participants then consumed a pre-determined MedDiet for 5 weeks. Both diets were consumed under weight-maintaining isoenergetic feeding conditions. Participants then underwent a 20-week free-living caloric restriction period, after which they consumed the MedDiet again in weight stabilizing, isoenergetic feeding conditions. RESULTS Body weight was reduced by 10.2%±2.9% and waist circumference by 8.6±3.3 cm after the weight loss period and stabilization on MedDiet (P<0.001). MedDiet-WL had no impact on plasma concentrations of leptin, plasminogen activator inhibitor-1, resistin, visfatin, acylation stimulating protein and adiponectin. MedDiet+WL reduced plasma leptin concentrations (P<0.01) and increased plasma adiponectin concentrations (P<0.05) compared with the control diet and MedDiet-WL. CONCLUSION Data from this nutritionally controlled study suggest that short-term consumption of MedDiet has little effect on the concentrations of many adipokines in the absence of weight loss.
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Affiliation(s)
- Caroline Richard
- Institute of Nutrition and Functional Foods, Laval University, 2440, boul. Hochelaga, Québec (Qc), Canada, G1V 0A6
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A single bout of downhill running transiently increases HOMA-IR without altering adipokine response in healthy adult women. Eur J Appl Physiol 2013; 113:2925-32. [PMID: 24068487 DOI: 10.1007/s00421-013-2717-5] [Citation(s) in RCA: 18] [Impact Index Per Article: 1.5] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 03/04/2013] [Accepted: 08/24/2013] [Indexed: 01/01/2023]
Abstract
PURPOSE Eccentric exercise-induced muscle damage may cause marked alterations in insulin sensitivity. However, it is not entirely known whether such alterations are also related to changes in adipokine levels. The aim of this study was to investigate the effects of muscle damage due to downhill running on inflammation, insulin sensitivity and selected adipokines related to insulin regulation (adiponectin, visfatin, resistin). METHODS Data were collected from 12 healthy adult women. Each subject participated in two trials, 4 weeks apart. The first trial was reserved for resting measurements only (control trial), while the second trial involved a 45-min exercise (-15 % slope, ~60 % of VO2max) intervention (exercise trial). Insulin sensitivity (HOMA), creatine kinase activity (CK), delayed onset muscle soreness (DOMS), tumor necrosis factor α (TNF-α), interleukin 6 (IL-6), glucose, insulin, adiponectin, resistin, and visfatin were assessed pre-exercise and 1, 2, 3, and 4 days post-exercise and during the same time points in the control trial. RESULTS Analyses revealed that CK, DOMS, TNF-α, IL-6, insulin and HOMA significantly increased (p < 0.05) throughout recovery (days 1-4). Adiponectin and visfatin remained unchanged, while resistin significantly increased (p < 0.05) only 2 days post-exercise. Visfatin was negatively correlated with HOMA at days 1 and 4 of recovery. CONCLUSION Although muscle damage due to downhill running caused a decline of insulin sensitivity, this response was not associated with the changes in adipokine levels.
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Periyalil HA, Gibson PG, Wood LG. Immunometabolism in obese asthmatics: are we there yet? Nutrients 2013; 5:3506-30. [PMID: 24025484 PMCID: PMC3798918 DOI: 10.3390/nu5093506] [Citation(s) in RCA: 21] [Impact Index Per Article: 1.8] [Reference Citation Analysis] [Abstract] [MESH Headings] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 07/01/2013] [Revised: 08/30/2013] [Accepted: 08/30/2013] [Indexed: 12/21/2022] Open
Abstract
Obesity is now recognised as a worldwide epidemic. The recent International Association for the Study of Obesity/International Obesity Taskforce (IASO/IOTF) analysis estimates that approximately 1.0 billion adults are currently overweight and a further 475 million are obese. Obesity has huge psychosocial impact with obese children and adolescents facing discrimination and stigmatization in many areas of their lives leading to body dissatisfaction, low self-esteem and depression. Indeed, obesity is recognised as an important risk factor for the development of several chronic diseases such as hypertension, cancer, asthma and metabolic syndrome. Chronic low grade systemic inflammation is considered as a hallmark of obesity and may possibly explain the link between obesity and chronic disease, in particular the increased incidence, prevalence and severity of asthma in obese individuals. There is now strong evidence for infiltration of immune and inflammatory cells into adipose tissue that drives systemic inflammation and subsequent end organ damage. In addition to adipocytes, the key adipose tissue resident immune cells are macrophages and mast cells. Immunometabolism, as an emerging field of investigation, explores the pivotal role of these immune cells in translating immunological changes to metabolic effects in obesity. Abundance of free fatty acids, along with other inflammatory cytokines shift the balance of metabolic homeostasis to pro-inflammatory status by influencing the development of inflammatory cell lineage, which, further exhibits distinct functional phenotypes. There is emerging evidence for macrophage activation and functional polarization of an anti-inflammatory M2 phenotype towards a pro-inflammatory M1 phenotype of macrophages in obese adipose tissue. Similarly, studies in both obese humans and murine models reveal the pathognomic presence of an increased number of mast cells in visceral adipose tissue. These suggest a possible contribution of mast cells to the unique metabolome of obese asthma. This review examines proposed multilevel interactions between metabolic and immune systems in obese asthmatics that underlie the negative effects of obesity and may offer significant therapeutic promise.
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Affiliation(s)
- Hashim A. Periyalil
- Priority Research Centre for Asthma and Respiratory Diseases, Faculty of Health, University of Newcastle, Callaghan, NSW 2308, Australia; E-Mails: (H.A.P.); (L.G.W.)
| | - Peter G. Gibson
- Priority Research Centre for Asthma and Respiratory Diseases, Faculty of Health, University of Newcastle, Callaghan, NSW 2308, Australia; E-Mails: (H.A.P.); (L.G.W.)
- Department of Respiratory and Sleep Medicine, Hunter Medical Research Institute, John Hunter Hospital, New Lambton, NSW 2305, Australia
- Author to whom correspondence should be addressed; E-Mail: or ; Tel.: +61-2-404-201-43; Fax: +61-2-404-200-46
| | - Lisa G. Wood
- Priority Research Centre for Asthma and Respiratory Diseases, Faculty of Health, University of Newcastle, Callaghan, NSW 2308, Australia; E-Mails: (H.A.P.); (L.G.W.)
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Asrih M, Jornayvaz FR. Inflammation as a potential link between nonalcoholic fatty liver disease and insulin resistance. J Endocrinol 2013; 218:R25-36. [PMID: 23833274 DOI: 10.1530/joe-13-0201] [Citation(s) in RCA: 217] [Impact Index Per Article: 18.1] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 12/13/2022]
Abstract
Nonalcoholic fatty liver disease (NAFLD) has become a major health problem in developed countries. It has affected more than 30% of the general population and is commonly associated with insulin resistance, which is a major risk factor for the development of type 2 diabetes and a central feature of the metabolic syndrome. Furthermore, accumulating evidences reveal that NAFLD as well as insulin resistance is strongly related to inflammation. Cytokines and adipokines play a pivotal role in inflammatory processes. In addition, these inflammatory mediators regulate various functions including metabolic energy balance, inflammation, and immune response. However, their role in modulating ectopic lipids involved in the development of insulin resistance, such as diacylglycerols and ceramides, remains unknown. The aim of this review is first to describe the pathophysiology of insulin resistance in NAFLD. In particular, we discuss the role of ectopic lipid accumulation in the liver. Secondly, we also summarize recent findings emphasizing the role of main inflammatory markers in both NAFLD and insulin resistance and their potential role in modulating hepatic fat content in NAFLD and associated hepatic insulin resistance.
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Affiliation(s)
- Mohamed Asrih
- Service of Endocrinology, Diabetes, Hypertension and Nutrition, Geneva University Hospital, Rue Gabrielle-Perret-Gentil 4, 1211 Genève 14, Switzerland
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Boulet LP. Asthma and obesity. Clin Exp Allergy 2013; 43:8-21. [PMID: 23278876 DOI: 10.1111/j.1365-2222.2012.04040.x] [Citation(s) in RCA: 130] [Impact Index Per Article: 10.8] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 06/30/2011] [Revised: 04/04/2012] [Accepted: 05/08/2012] [Indexed: 12/12/2022]
Abstract
The prevalence and incidence of asthma have increased among obese children and adults, particularly among women. Obesity seems to be a predisposing factor for the development of asthma, but the underlying mechanisms of its influence are still uncertain. Various hypotheses have been proposed to explain the link between obesity and asthma such as a common genetic predisposition, developmental changes, altered lung mechanics, the presence of a systemic inflammatory process, and an increased prevalence of associated comorbid conditions. Over-diagnosis of asthma does not seem to be more frequent in obese compared to non-obese subjects, but the added effects of obesity on respiratory symptoms can affect asthma control assessment. Obesity can make asthma more difficult to control and is associated with a reduced beneficial effect of asthma medications. This could be due to a change in asthma phenotype, particularly evidenced as a less eosinophilic type of airway inflammation combined to the added effects of changes in lung mechanics. Weight loss is associated with a universal improvement of asthma and should be part of asthma management in the obese patient. Additional research should be conducted to better determine how obesity influences the development and clinical expression of asthma, establish the optimal management of asthma in this population and determine how obesity affects long-term asthma outcomes in these patients.
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Affiliation(s)
- L-P Boulet
- Institut universitaire de cardiologie et de pneumologie de Québec, Laval University, Québec, QC, Canada.
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Barber TM, Franks S. Adipocyte biology in polycystic ovary syndrome. Mol Cell Endocrinol 2013; 373:68-76. [PMID: 23084978 DOI: 10.1016/j.mce.2012.10.010] [Citation(s) in RCA: 54] [Impact Index Per Article: 4.5] [Reference Citation Analysis] [Abstract] [MESH Headings] [Grants] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 05/21/2012] [Accepted: 10/05/2012] [Indexed: 01/23/2023]
Abstract
Polycystic Ovary Syndrome (PCOS) is a common endocrinopathy that is associated with an adverse metabolic profile including insulin resistance. There is a clear association between obesity, the development of PCOS and the severity of its phenotypic, biochemical and metabolic features. Evidence to support this link includes data from epidemiological, pathophysiological and genetic studies. Given the importance of obesity in the development and manifestation of PCOS, ongoing research into the many facets of adipocyte biology in women with the condition is important and should continue to be a priority. In this review article, we discuss the existing literature on fat distribution, adipokines, adipocyte hypertrophy and adipocyte steroid metabolism in women with PCOS.
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Affiliation(s)
- T M Barber
- Warwickshire Institute for the Study of Diabetes, Endocrinology and Metabolism, University of Warwick, Coventry CV2 2DX, United Kingdom.
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Du X, He S, Jiang Y, Wei L, Hu W. Adiponectin prevents islet ischemia-reperfusion injury through the COX2-TNFα-NF-κB-dependent signal transduction pathway in mice. J Endocrinol 2013; 218:75-84. [PMID: 23589741 DOI: 10.1530/joe-12-0568] [Citation(s) in RCA: 24] [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] [Indexed: 12/30/2022]
Abstract
Islets are exceptionally susceptible to ischemia-reperfusion injury, an increased incidence of primary graft nonfunctionality, and β-cell death during a transplant procedure. Therefore, islets require protection during the early stages of the transplant procedure. Based on the beneficial vascular and anti-inflammatory activity of adiponectin, we hypothesize that adiponectin protects islet cells against ischemia-reperfusion injury and graft dysfunction after transplantation. To examine the effects of adiponectin on the resistance of islet ischemia-reperfusion injury, we used the islet hypoxia-reoxygenation injury model and performed kidney subcapsular syngeneic islet transplants to assess the islets' vitality and function. Furthermore, we utilized lipopolysaccharide (LPS)-induced or tumor necrosis factor α (TNFα)-induced damage to islet cells to model the inflammation of post-transplant ischemia-reperfusion injury and transplanted islets in adiponectin knockout mice to explore whether the protective action of adiponectin is involved in TNFα production and nuclear transcription factor-κB (NF-κB) activation. Adiponectin suppressed TNFα production and IκB-α phosphorylation; decreased hypoxia-reoxygenation and LPS-induced and TNFα-induced islet apoptosis; and improved islet function in vivo and in vitro. Our results demonstrate that adiponectin protects the islet from injury. We show that islet protection occurs in response to ischemia-reperfusion and is dependent on the suppression of islet production by TNFα through cyclooxygenase 2 and the inhibition of the TNFα-induced NF-κB activation pathways.
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Affiliation(s)
- Xiaojiong Du
- Department of Hepatobiliopancreatic Surgery, Laboratory of Transplant Engineering and Immunology, Regenerative Medicine Research Center and Department of Emergency, West China Hospital, Sichuan University, No. 37 Guoxuexiang, Wuhou District, Chengdu, Sichuan Province 610041, People's Republic of China
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Moghadasi M, Mohebbi H, Rahmani-Nia F, Hassan-Nia S, Noroozi H. Effects of short-term lifestyle activity modification on adiponectin mRNA expression and plasma concentrations. Eur J Sport Sci 2013; 13:378-85. [DOI: 10.1080/17461391.2011.635701] [Citation(s) in RCA: 14] [Impact Index Per Article: 1.2] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 01/22/2023]
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Matsuda M, Tamura R, Kishida N, Segawa T, Kanno K, Nishimoto O, Nakamoto K, Nishiyama H, Kawamoto T. Predictive value of adiponectin in patients with multivessel coronary atherosclerosis detected on computed tomography angiography. J Atheroscler Thromb 2013; 20:767-76. [PMID: 23759798 DOI: 10.5551/jat.18036] [Citation(s) in RCA: 13] [Impact Index Per Article: 1.1] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 11/11/2022] Open
Abstract
AIM Multislice computed tomography coronary angiography (CTCA) can be used to detect coronary plaques that predict the risk of cardiovascular events. This study aimed to identify the risk factors associated with the extent of coronary plaques detected using CTCA and to determine the value of adiponectin measurement for identifying high-risk patients with multivessel coronary atherosclerosis. METHODS The study included 298 patients who underwent CTCA for coronary artery disease (CAD) screening between July 2008 and October 2011. We investigated the relationship between the extent of coronary atherosclerosis in terms of the number of diseased vessels and various risk factors, including the serum adiponectin level. RESULTS The adiponectin level was found to be significantly associated with multivessel coronary atherosclerosis in a univariate analysis (p=0.001). A multivariate analysis revealed the adiponectin level to also be significantly associated with multivessel coronary atherosclerosis (p=0.01), independent of other significant risk factors, including an advanced age, male gender, diabetes mellitus (DM) and hypertension (HT). A receiver operating characteristic curve analysis revealed that a combination of these factors significantly predicted multivessel coronary atherosclerosis (area under the curve, 0.73;95% confidence interval, 0.67-0.78). As the number of these factors increased, the proportion of patients with multivessel coronary atherosclerosis increased, while the proportion of patients with normal coronary arteries decreased (p < 0.0001). CONCLUSIONS A low adiponectin level combined with an advanced age, male gender, DM, and HT is independently and incrementally associated with multivessel coronary atherosclerosis. The number of factors may predict the extent of coronary atherosclerosis in patients without documented CAD.
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Affiliation(s)
- Morihiro Matsuda
- Department of Cardiology, National Hospital Organization, Kure Medical Center Chugoku Cancer Center
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Dietary Supplementation of Calcium may Counteract Obesity in Mice Mediated by Changes in Plasma Fatty Acids. Lipids 2013; 48:817-26. [DOI: 10.1007/s11745-013-3798-y] [Citation(s) in RCA: 11] [Impact Index Per Article: 0.9] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 03/08/2013] [Accepted: 05/08/2013] [Indexed: 12/28/2022]
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Hwang JY, Park JE, Choi YJ, Huh KB, Chang N, Kim WY. Carbohydrate Intake Interacts With SNP276G>T Polymorphism in the Adiponectin Gene to Affect Fasting Blood Glucose, HbA1C, and HDL Cholesterol in Korean Patients With Type 2 Diabetes. J Am Coll Nutr 2013; 32:143-50. [DOI: 10.1080/07315724.2013.791795] [Citation(s) in RCA: 9] [Impact Index Per Article: 0.8] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 01/08/2023]
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de Luis D, Aller R, Izaola O, Conde R, de la Fuente B, Gonzalez Sagrado M. Genetic variation in the endocannabinoid degrading enzyme fatty acid amide hydrolase (FAAH) and their influence on weight loss and insulin resistance under a high monounsaturated fat hypocaloric diet. J Diabetes Complications 2013; 27:235-9. [PMID: 23333123 DOI: 10.1016/j.jdiacomp.2012.11.001] [Citation(s) in RCA: 9] [Impact Index Per Article: 0.8] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 09/04/2012] [Revised: 10/16/2012] [Accepted: 11/06/2012] [Indexed: 10/27/2022]
Abstract
BACKGROUND AND AIMS The C385A polymorphism of FAAH gene (rs324420C>A) has been associated with obesity. We investigate the role of this polymorphism on anthropometric and metabolic responses after an enriched monounsaturated fat hypocaloric diet. METHODS A sample of 95 obese individuals was analyzed at baseline and after 3 months of an enriched monounsaturated fat hypocaloric diet. RESULTS Sixty two patients (65.3%) had the genotype C385C and 33 (34.7%) patients had C385A genotype (30 patients, 31.6%) or A358A (3 patients, 3.2%) (A carriers group). In subjects with C385C genotype, insulin (-1.9±5.3 mUI/l) and HOMA-R (-0.48±0.75 U) decreased. In A carriers subjects, the decreases in weight were 3.7±3.4 kg (decrease in C385C genotype group 4.4±3.6 kg), fat mass 2.7±3.2 kg (decrease in C385C genotype group 3.4±3.2 kg) and waist circumference 3.1±3.4cm (decrease in C385 genotype group 4.4±4.6 cm). These changes were significantly higher in the C385C genotype group than the A carriers subjects. CONCLUSION After weight loss, noncarriers of the allele A385 of FAAH had an improvement on insulin and HOMA-R levels with an enriched monounsaturated fat hypocaloric diet. A better response of weight, fat mass and waist circumference was observed in C385 genotype subjects than A carriers participants.
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Affiliation(s)
- Daniel de Luis
- Institute of Endocrinology and Nutrition, Medicine School and Unit of Investigation, Hospital Rio Hortega, University of Valladolid, C/Los perales 16, Simancas 47130, Valladolid, Spain.
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Golbidi S, Laher I. Potential mechanisms of exercise in gestational diabetes. J Nutr Metab 2013; 2013:285948. [PMID: 23691290 PMCID: PMC3649306 DOI: 10.1155/2013/285948] [Citation(s) in RCA: 19] [Impact Index Per Article: 1.6] [Reference Citation Analysis] [Abstract] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 09/25/2012] [Revised: 01/31/2013] [Accepted: 02/10/2013] [Indexed: 02/07/2023] Open
Abstract
Gestational diabetes mellitus (GDM) is defined as glucose intolerance first diagnosed during pregnancy. This condition shares same array of underlying abnormalities as occurs in diabetes outside of pregnancy, for example, genetic and environmental causes. However, the role of a sedentary lifestyle and/or excess energy intake is more prominent in GDM. Physically active women are less likely to develop GDM and other pregnancy-related diseases. Weight gain in pregnancy causes increased release of adipokines from adipose tissue; many adipokines increase oxidative stress and insulin resistance. Increased intramyocellular lipids also increase cellular oxidative stress with subsequent generation of reactive oxygen species. A well-planned program of exercise is an important component of a healthy lifestyle and, in spite of old myths, is also recommended during pregnancy. This paper briefly reviews the role of adipokines in gestational diabetes and attempts to shed some light on the mechanisms by which exercise can be beneficial as an adjuvant therapy in GDM. In this regard, we discuss the mechanisms by which exercise increases insulin sensitivity, changes adipokine profile levels, and boosts antioxidant mechanisms.
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Affiliation(s)
- Saeid Golbidi
- Department of Pharmacology and Therapeutics, Faculty of Medicine, University of British Columbia, Vancouver, BC, Canada V6T 1Z3
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Aged garlic extract improves adiponectin levels in subjects with metabolic syndrome: a double-blind, placebo-controlled, randomized, crossover study. Mediators Inflamm 2013; 2013:285795. [PMID: 23533302 PMCID: PMC3603419 DOI: 10.1155/2013/285795] [Citation(s) in RCA: 43] [Impact Index Per Article: 3.6] [Reference Citation Analysis] [Abstract] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 01/10/2013] [Accepted: 01/31/2013] [Indexed: 12/25/2022] Open
Abstract
BACKGROUND Garlic (Allium sativum) has been shown to have important benefits in individuals at high cardiovascular risk. The aim of the present study was to evaluate the effects of the administration of aged garlic extract (AGE) on the risk factors that constitute the cluster of metabolic syndrome (MS). METHODS AND DESIGN Double-blind, crossover, randomized, placebo-controlled clinical trial to assess the effect of 1.2 g/day of AGE (Kyolic), for 24 weeks of treatment (12 weeks of AGE and 12 weeks of placebo), on subjects with MS. RESULTS The administration of AGE increased the plasma levels of adiponectin (P = 0.027). No serious side effects associated with the intervention were reported. CONCLUSION The present results have shown for the first time that the administration of AGE for 12 weeks increased plasma adiponectin levels in patients with MS. This suggests that AGE might be a useful, novel, nonpharmacological therapeutic intervention to increase adiponectin and to prevent cardiovascular (CV) complications in individuals with MS.
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Lee CY, Jan MS, Yu MC, Lin CC, Wei JCC, Shih HC. Relationship between Adiponectin and Leptin, and Blood Lipids in Hyperlipidemia Patients Treated with Red Yeast Rice. ACTA ACUST UNITED AC 2013; 20:197-203. [DOI: 10.1159/000351455] [Citation(s) in RCA: 9] [Impact Index Per Article: 0.8] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 11/19/2022]
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Gemfibrozil and its combination with metformin on pleiotropic effect on IL-10 and adiponectin and anti-atherogenic treatment in insulin resistant type 2 diabetes mellitus rats. Inflammopharmacology 2012; 21:137-45. [DOI: 10.1007/s10787-012-0154-4] [Citation(s) in RCA: 8] [Impact Index Per Article: 0.6] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 05/27/2012] [Accepted: 10/08/2012] [Indexed: 11/25/2022]
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Abstract
Adipocytokines are primarily adipocyte-derived products, although certain members are also synthesized by other cell types. These adipocytokines, similarly to classical cytokines, are characterized by very pleiotropic functions affecting biological processes throughout the body. An increasing number of adipocytokines has recently been recognized, such as adiponectin, leptin, pre-B cell colony-enhancing factor/Nampt/visfatin, resistin, progranulin, and others. Adiponectin has emerged as the most abundant circulating adipocytokine, is produced almost exclusively by adipocytes, and has mainly anti-inflammatory and anti-diabetic functions. In contrast, leptin is produced by many cell types beyond adipocytes, regulates immunity and T cell functions, and acts in a more pro-inflammatory fashion. Adipocytokines play a fundamental role in adipose tissue homeostasis (i.e. health) and disease, especially in obesity-related disorders such as non-alcoholic fatty liver diseases (NAFLD) and their complications, including hepatocellular carcinoma (HCC). Lack of adiponectin as observed in NAFLD drives steatosis and inflammation in the liver, and evidence is increasing that this adipocytokine has many anti-tumor properties and might play a rather protective role in HCC. The role of leptin in NAFLD is still unclear and this adipocytokine seems to have opposite effects in HCC, acting more as a tumor promoter. Evidence is increasing that HCC tissue produces various adipocytokines, and adiponectin expression in HCC seems to be decreased whereas leptin expression is rather increased. In conclusion, adipocytokines are increasingly recognized as pleiotropic molecules involved in the pathophysiology of HCC, which might lead to therapeutic approaches targeting these mediators.
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Affiliation(s)
- Verena Wieser
- Christian Doppler Research Laboratory for Gut Inflammation, Innsbruck Medical University, Austria
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Kumagai S, Kishimoto H, Zou B. The leptin to adiponectin ratio is a good biomarker for the prevalence of metabolic syndrome, dependent on visceral fat accumulation and endurance fitness in obese patients with diabetes mellitus. Metab Syndr Relat Disord 2012; 3:85-94. [PMID: 18370715 DOI: 10.1089/met.2005.3.85] [Citation(s) in RCA: 15] [Impact Index Per Article: 1.2] [Reference Citation Analysis] [Abstract] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 01/25/2023] Open
Abstract
BACKGROUND We investigated the contribution of adiponectin or leptin on the prevalence of metabolic syndrome (MS), while also taking cardiorespiratory fitness and visceral fat accumulation into account regarding diabetes patients. METHODS Japanese male patients (n = 77) with either impaired glucose tolerance (IGT) or type 2 diabetes mellitus were divided into three tertiles according to their adipocytokine levels. A logistic regression analysis was performed after adjusting for age to investigate the association between the adipocytokine levels and the prevalence of MS based on World Health Organization (WHO) criteria. RESULTS The visceral fat area (VFA) and maximal oxygen uptake ([Formula: see text] O(2)max) were found to be significantly different within the tertiles regarding the leptin and adiponectin levels and the adiponectin-to-leptin (A/L) ratio. The low tertile of leptin showed a significantly lower odds ratio (OR) for prevalence of MS than that in the high group. Both the low and the medium tertiles of adiponectin showed a significantly higher OR for prevalence of SM than that of the high group. Especially, the low tertile of A/L ratio had about an eight times higher prevalence of MS than the high tertile, and the difference was significant. However, when both the VFA and/or [Formula: see text] O(2)max were added to the logistic regression model as adjusting factors, all of these significant differences disappeared. CONCLUSION The A/L ratio is suggested to be a good biomarker for the prevalence of MS in comparison to the adiponectin and leptin levels alone. However, these relationships are dependent on abdominal fat accumulation and/or cardiorespiratory fitness levels.
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Affiliation(s)
- Shuzo Kumagai
- Institute of Health Science, Fukuoka University, Fukuoka, Japan
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Seshadri P, Samaha FF, Stern L, Ahima RS, Daily D, Iqbal N. Adipocytokine changes caused by low-carbohydrate compared to conventional diets in obesity. Metab Syndr Relat Disord 2012; 3:66-74. [PMID: 18370712 DOI: 10.1089/met.2005.3.66] [Citation(s) in RCA: 17] [Impact Index Per Article: 1.3] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 11/12/2022] Open
Abstract
Modest weight loss causing a decrease in insulin resistance has been linked to favorable changes in the adipocyte cytokines leptin, adiponectin, and tumor necrosis factor-alpha (TNF-alpha), three emerging risk factors of cardiovascular disease. We previously observed a significant reduction in insulin resistance with weight loss in obese subjects on a low-carbohydrate diet. Based on these previous findings, we hypothesize that a low-carbohydrate diet would be more beneficial in changing leptin, TNF-alpha, and adiponectin than a conventional diet. A total of 75 severely obese (body mass index >/=35 kg/m(2)) subjects were randomized to instruction of 6 months of a low-carbohydrate diet or a conventional calorie-restricted diet. Serum levels of leptin, TNF-alpha, TNF-alpha-soluble receptor 1 (TNF-alpha SR1), and adiponectin were measured at baseline and after 6 months of dietary intervention. Subjects on low-carbohydrate diets experienced a greater decrease in leptin when compared to conventional dieters (p < 0.001). TNF-alpha increased significantly in nondiabetic subjects on conventional vs. low-carbohydrate diets (p = 0.003). Adiponectin and TNF-alpha SR1 change were not significantly different between diets. This is the first study to report the effects of dietary macronutrient alterations on serum adipocytokines in a randomized controlled trial. The greater reduction in insulin resistance and weight on a low-carbohydrate diet, in the short term, translates into greater improvement in leptin but with no significant improvements in TNF-alpha or adiponectin in patients with moderate to severe obesity after 6 months of dietary intervention.
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Affiliation(s)
- Prakash Seshadri
- Division of Endocrinology, Department of Medicine, University of Pennsylvania Medical School, Philadelphia, Pennsylvania., Department of Medicine, Veterans Affairs Medical Center, Philadelphia, Pennsylvania
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Brock CM, King DS, Wofford MR, Harrell TK. Exercise, insulin resistance, and hypertension: a complex relationship. Metab Syndr Relat Disord 2012; 3:60-5. [PMID: 18370711 DOI: 10.1089/met.2005.3.60] [Citation(s) in RCA: 16] [Impact Index Per Article: 1.2] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 01/22/2023] Open
Abstract
More than 300,000 deaths occur annually in the United States alone as a result of obesity, poor dietary habits, or physical inactivity. Obesity is now an increasingly recognized independent risk factor for cardiovascular disease and leads to numerous other comorbidities. The causal relationships between obesity and both insulin resistance and hypertension have been consistently demonstrated in numerous studies. The relationships consist of cascading events involving insulin, leptin, adiponectin, and other hormones that often precipitate the development of metabolic syndrome. As we learn more about the metabolic activity of the adipose tissue, we can better identify the mechanisms that associate weight reduction with a decrease in health risks. Evidence suggests that exercise produces a positive effect on weight reduction, insulin sensitivity, and blood pressure. Therefore, weight reduction and therapeutic changes in lifestyle should be encouraged in all overweight and obese patients. It is imperative to increase the awareness of the obesity epidemic and to emphasize the importance of exercise as both treatment and prevention of metabolic disease.
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Affiliation(s)
- Cori M Brock
- University of Mississippi Medical Center, Department of Pharmacy, Jackson, Mississippi
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Idorn T, Hornum M, Bjerre M, Jørgensen KA, Nielsen FT, Hansen JM, Flyvbjerg A, Feldt-Rasmussen B. Plasma adiponectin before and after kidney transplantation. Transpl Int 2012; 25:1194-203. [PMID: 22994569 DOI: 10.1111/j.1432-2277.2012.01560.x] [Citation(s) in RCA: 13] [Impact Index Per Article: 1.0] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 12/31/2022]
Abstract
The role of plasma adiponectin (ADPN) in patients with impaired kidney function and following kidney transplantation (Tx) is debated. We aimed to: (i) determine whether pretransplant ADPN level is an independent risk factor for deterioration of glucose tolerance including development of new-onset diabetes mellitus after Tx, (ii) describe which parameters that influence the ADPN concentration before and after Tx. Fifty-seven nondiabetic kidney allograft recipients and 40 nondiabetic uraemic patients were included. The Tx group was examined at baseline and 3 and 12 months after Tx. The uraemic control group was examined twice, separated by 12 months. ADPN levels declined significantly following Tx (P < 0.0001), while estimated glomerular filtration rate (eGFR) increased (P < 0.0005). eGFR, BMI and insulin sensitivity index were independently associated with ADPN in a multivariate regression analysis, whereas an ordinal logistic regression analysis revealed no predictive characteristic of ADPN for aggravation of the glucose tolerance after Tx. In conclusion, kidney transplantation is accompanied by a significant reduction in ADPN concentration. Several factors determine the ADPN concentration before and after Tx including kidney function, insulin resistance, use of immunosuppressive agents and BMI. Pretransplant ADPN level did not predict development of new-onset diabetes mellitus or even deterioration of the glucose tolerance following Tx.
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Affiliation(s)
- Thomas Idorn
- Department of Nephrology, Copenhagen University Hospital, Rigshospitalet, Copenhagen, Denmark.
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Harwood HJ. The adipocyte as an endocrine organ in the regulation of metabolic homeostasis. Neuropharmacology 2012; 63:57-75. [DOI: 10.1016/j.neuropharm.2011.12.010] [Citation(s) in RCA: 185] [Impact Index Per Article: 14.2] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 09/26/2011] [Revised: 11/28/2011] [Accepted: 12/09/2011] [Indexed: 02/06/2023]
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Bikman BT. A role for sphingolipids in the pathophysiology of obesity-induced inflammation. Cell Mol Life Sci 2012; 69:2135-46. [PMID: 22294100 PMCID: PMC11114706 DOI: 10.1007/s00018-012-0917-5] [Citation(s) in RCA: 54] [Impact Index Per Article: 4.2] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 11/01/2011] [Revised: 01/01/2012] [Accepted: 01/04/2012] [Indexed: 12/20/2022]
Abstract
Following the initial discovery that adipose tissue actively synthesizes and secretes cytokines, obesity-induced inflammation has been implicated in the etiology of a host of disease states related to obesity, including cardiovascular disease and type II diabetes. Interestingly, a growing body of evidence similarly implicates sphingolipids as prime instigators in these same diseases. From the recent discovery that obesity-related inflammatory pathways modulate sphingolipid metabolism comes a novel perspective—sphingolipids may act as the dominant mediators of deleterious events stemming from obesity-induced inflammation. This paradigm may identify sphingolipids as an effective target for future therapeutics aimed at ameliorating diseases associated with chronic inflammation.
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Affiliation(s)
- Benjamin T Bikman
- Department of Physiology and Developmental Biology, Brigham Young University, Provo, UT 84602, USA.
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Adiponectin, Non-Esterified Fatty Acids and Antiphospholipid Antibodies in Type II Diabetes Mellitus. J Med Biochem 2012. [DOI: 10.2478/v10011-012-0009-y] [Citation(s) in RCA: 2] [Impact Index Per Article: 0.2] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 11/20/2022] Open
Abstract
Adiponectin, Non-Esterified Fatty Acids and Antiphospholipid Antibodies in Type II Diabetes MellitusThe importance of the association of antiphospholipid antibodies (aPL Abs) with the features of type II diabetes mellitus has not yet been elucidated. The aim of this work was to investigate the association of aPL Abs with adiponectin and non-esterified fatty acids (NEFA) in type II diabetes mellitus patients without micro and/or macrovascular complications, and to analyze the differences between the male and female patients with regard to the abovementioned parameters. Male patients with type II diabetes mellitus showed a positive correlation between NEFA concentrations and anti-oxLDL antibodies (r=0.334, p=0.019). A weak, but statistically significant correlation between adiponectin concentrations and the IgM isotype of anti-annexin A5 antibodies was found in type II diabetes mellitus patients (r=0.285, p=0.011). The presence of a positive correlation between NEFA and anti-oxLDL antibodies might be useful in the detection of patients with premature atherosclerosis in type II diabetes mellitus patients without any micro and/or macrovascular complications among type II diabetes mellitus patients.
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Schwetz V, Pieber T, Obermayer-Pietsch B. The endocrine role of the skeleton: background and clinical evidence. Eur J Endocrinol 2012; 166:959-67. [PMID: 22436399 DOI: 10.1530/eje-12-0030] [Citation(s) in RCA: 70] [Impact Index Per Article: 5.4] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 12/19/2022]
Abstract
Based on the observation that diabetes, obesity, and hypogonadism influence bone metabolism, the existence of a feedback loop and a common regulation was postulated and an endocrine role ascribed to the skeleton. In the first part of this review, two pathways are described whereby adipose tissue acts on bone mass. In the first, leptin activates the sympathetic nervous system via serotonin and diminishes bone mass accrual. The second pathway functions via the activation of CART (CARTPT) and inhibits bone resorption. The first pathway leads to a decrease in bioactivity of the osteoblast-produced hormone osteocalcin (OC) (part 2). In its undercarboxylated form, OC acts on the three targets pancreas, adipose tissue, and gonads (part 3) and thereby causes an increase in insulin secretion and sensitivity, β-cell proliferation, and male fertility. Insulin (part 4) is part of a recently discovered regulatory feedback loop between pancreas and osteoblasts. It is a strong counterplayer of leptin as it causes a decrease in OPG expression and enhances bone resorption and OC decarboxylation. Numerous clinical studies (part 5) have shown associations of total and undercarboxylated OC and markers of energy metabolism. Interventional studies, to date only performed in murine models, have shown positive effects of OC administration on energy metabolism. Whether bone tissue has an even further-reaching endocrine role remains to be elucidated.
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Affiliation(s)
- Verena Schwetz
- Division of Endocrinology and Metabolism, Department of Internal Medicine, Medical University of Graz, Auenbruggerplatz 15, Graz, Austria
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Abstract
UNLABELLED The global epidemic of obesity is accompanied by an increased prevalence of cardiovascular disease (CVD), in particular stroke and heart attack. Dysfunctional adipose tissue links obesity to CVD by secreting a multitude of bioactive lipids and pro-inflammatory factors (adipokines) with detrimental effects on the cardiovascular system. Adiponectin is one of the few adipokines that possesses multiple salutary effects on insulin sensitivity and cardiovascular health. Clinical investigations have identified adiponectin deficiency (hypoadiponectinaemia) as an independent risk factor for CVD. In animals, elevation of plasma adiponectin by either pharmacological or genetic approaches alleviates obesity-induced endothelial dysfunction and hypertension, and also prevents atherosclerosis, myocardial infarction and diabetic cardiomyopathy. Furthermore, many therapeutic benefits of the peroxisome-proliferator activated receptor gamma agonists, the thiazolidinediones, are mediated by induction of adiponectin. Adiponectin protects cardiovascular health through its vasodilator, anti-apoptotic, anti-inflammatory and anti-oxidative activities in both cardiac and vascular cells. This review summarizes recent findings in the understanding of the physiological role and clinical relevance of adiponectin in cardiovascular health, and in the identification of the receptor and postreceptor signalling events that mediate the cardiovascular actions of adiponectin. It also discusses adiponectin-targeted drug discovery strategies for treating obesity, diabetes and CVD. 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)
- Xiaoyan Hui
- Department of Medicine, the University of Hong Kong, Hong Kong
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Teplan V, Malý J, Gürlich R, Teplan V, Kudla M, Pit'ha J, Racek J, Haluzík M, Senolt L, Stollová M. Muscle and fat metabolism in obesity after kidney transplantation: no effect of peritoneal dialysis or hemodialysis. J Ren Nutr 2012; 22:166-70. [PMID: 22200436 DOI: 10.1053/j.jrn.2011.10.016] [Citation(s) in RCA: 9] [Impact Index Per Article: 0.7] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 10/07/2011] [Accepted: 10/13/2011] [Indexed: 11/11/2022] Open
Abstract
Our prospective study analyzed selected adipocytokines: adiponectin (ADPN), leptin, visfatin, and asymmetric dimethylarginine (ADMA) in the plasma of renal transplant recipients previously treated by peritoneal dialysis and hemodialysis. A total of 70 patients were on follow-up for 12 months after transplantation. Of these, 30 patients (group I) developed obesity, and 40 patients were nonobese (group II). All were receiving standard immunosuppressive therapy (cyclosporine A or tacrolimus and mycophenolate mofetil, with prednisone added in the early posttransplant period) and did not differ statistically in HLA typing, age, sex, duration of previous dialysis, history of cardiovascular disease, and rate of rejection episodes. At the end of the study period, there were significant differences between groups I and II (t test, analysis of variance) in plasma: ADPN, 22.30 ± 10.2 versus 14.3 ± 7.2 μg/mL; visfatin, 1.7 ± 0.1 versus 1.2 ± 0.1 ng/mL; ADMA, 3.60 ± 0.47 versus 2.10 ± 0.36 μmol/L; P < .01; leptin, 55.6 ± 10.2 versus 25.6 ± 8.3 ng/L; P < .01 (P < .02). In conclusion, an increase of body fat after renal transplantation was associated with an increase of ADMA and leptin, TNF-α, MCP-1, and visfatin and decrease of adiponectin. Our study documented there was now long-term beneficial metabolic effect of peritoneal dialysis in developing posttransplant obesity.
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Affiliation(s)
- Vladimír Teplan
- Department of Nephrology, Transplant Centre, Institute for Clinical and Experimental Medicine, Prague, Czech Republic.
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Ata SM, Vaishnav U, Puglisi M, Lofgren IE, Wood RJ, Volek JS, Fernandez ML. Macronutrient composition and increased physical activity modulate plasma adipokines and appetite hormones during a weight loss intervention. J Womens Health (Larchmt) 2012; 19:139-45. [PMID: 20088670 DOI: 10.1089/jwh.2009.1472] [Citation(s) in RCA: 17] [Impact Index Per Article: 1.3] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 01/14/2023] Open
Abstract
BACKGROUND We have shown previously that in overweight premenopausal women, changes in macronutrient composition and increasing the number of steps walked per day favorably affect body composition and plasma lipid profiles. As a follow-up, we evaluated the effect of moderate carbohydrate intake and increased physical activity on inflammation and regulation of appetite. METHODS Seventy premenopausal women with a body mass index (BMI) between 25 and 37 kg/m(2) participated in a 10-week weight loss intervention program consisting of the following macronutrient energy distribution: 40% carbohydrate, 30% fat, and 30% protein, in addition to a progressive increase in the number of steps taken per day. Plasma adiponectin, intracellular adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule-1 (VCAM-1), leptin, and ghrelin levels were assessed at baseline and after 10 weeks. RESULTS Subjects reduced body weight by 4.5%, waist circumference (WC) by 6.4%, and trunk fat by 4.6%. Plasma insulin and insulin resistance assessed by homeostasis model assessment (HOMA) were reduced after 10 weeks (p < 0.01). Plasma adiponectin was increased by 11% (p < 0.05), and ICAM-1 levels were decreased (p < 0.05) after 10 weeks. A negative correlation was found between changes in insulin and changes in adiponectin between baseline and 10 weeks (r = -0.397, p < 0.01), indicating a role of adiponectin in increasing insulin sensitivity. In addition, plasma ghrelin levels were increased by 17% (p < 0.001), indicating a signal for increased appetite associated with weight loss. CONCLUSIONS These studies indicate that weight loss interventions involving moderate changes in dietary carbohydrate and increases in physical activity favorably affect insulin sensitivity and decrease inflammation.
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Affiliation(s)
- Shymaa M Ata
- Department of Nutritional Sciences, University of Connecticut, Storrs, Connecticut 06269, USA
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Singh A, Krishna A. Localization of adiponectin and its receptor and its possible roles in the ovary of a vespertilionid bat, Scotophilus heathi. Gen Comp Endocrinol 2012; 176:240-51. [PMID: 22342274 DOI: 10.1016/j.ygcen.2012.01.020] [Citation(s) in RCA: 14] [Impact Index Per Article: 1.1] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 10/28/2011] [Revised: 01/02/2012] [Accepted: 01/29/2012] [Indexed: 02/06/2023]
Abstract
The aim of this study was to evaluate the seasonal variation in serum adiponectin levels and ovarian expression of adiponectin and its receptor in the Scotophilus heathi bat and their relationship to the changes in the body fat mass, serum insulin and luteinizing hormone (LH) levels, and ovarian activity. A very high level of circulating adiponectin was found during recrudescence, whereas a very low level of circulating adiponectin was observed during pre-ovulatory period. The increased circulating adiponectin level coincided with fat deposition, insulin resistance and hyperinsulinemia (HI) in S. heathi. Immunocytochemical study in the ovary of bat showed localization of adiponectin mainly in thecal-interstitial cells (TICs), and adiponectin receptor 1 (AdipoR1) in the granulosa cells of growing follicles, but showed no staining in atretic follicle. Seasonal changes in ovarian adiponectin and AdipoR1 levels showed two peaks (during recrudescence and ovulatory phases) coinciding with two periods of follicular development. Adiponectin in the absence of LH, as occur during recrudescence, stimulates androstenedione (A4) synthesis in vitro by up-regulating the insulin receptor (IR). Adiponectin in presence of LH, as occur during pre-ovulatory phase, inhibits A4 synthesis in vitro by down-regulating androgen receptor (AR). Further, the in vitro study showed that adiponectin, in presence of LH, also promotes luteinizing hormone receptor (LH-R) and steroidogenic acute regulatory protein (StAR) level in the ovary, which might help in development of ovulatory follicles. In brief, adiponectin in the absence of LH induces increased A4 synthesis and consequently the condition of delayed ovulation, whereas in the presence LH suppresses both synthesis and action of A4 and thus induces preovulatory condition in the ovary of S. heathi.
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Affiliation(s)
- Ajit Singh
- Department of Zoology, Banaras Hindu University, Varanasi 221 005, India
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Hall AC, Fairclough AC, Mahadevan K, Paxman JR. Ascophyllum nodosum enriched bread reduces subsequent energy intake with no effect on post-prandial glucose and cholesterol in healthy, overweight males. A pilot study. Appetite 2012; 58:379-86. [PMID: 22100188 DOI: 10.1016/j.appet.2011.11.002] [Citation(s) in RCA: 46] [Impact Index Per Article: 3.5] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 03/23/2011] [Revised: 08/12/2011] [Accepted: 11/03/2011] [Indexed: 10/15/2022]
Abstract
It is well recognised that the consumption of seaweed isolates (such as alginate) successfully reduce energy intake and modulate glycaemic and cholesterolaemic responses. However, to date, the effect of adding whole seaweed to bread has not been widely investigated. Hence, this study aims to investigate the acceptability of Ascophyllum nodosum enriched bread as part of a meal, and measure its effect on energy intake and nutrient absorption in overweight, healthy males to see if it has a similar impact. Results from the acceptability study, (79 untrained sensory panellists) indicated that it is acceptable to incorporate seaweed (A. nodosum) into a staple food such as bread at concentrations of up to 4% per 400 g wholemeal loaf. A single blind cross over trial (n=12 males, aged 40.1±12.5 years; BMI 30.8±4.4 kg/m(2)) was used to compare energy intake and nutrient uptake after a breakfast meal using the enriched bread (4% A. nodosum) against the control bread (0% A. nodosum). Consumption of the enriched bread at breakfast led to a significant reduction (16.4%) in energy intake at a test meal 4 h later. Differences between treatment arms for area under the curve, peak values, and time of peak for blood glucose and cholesterol were not significant. Further investigation of potential mechanisms of action is warranted.
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Affiliation(s)
- A C Hall
- Centre for Food Innovation, Sheffield Business School, City Campus, Howard Street, Sheffield S1 1WB, United Kingdom.
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Nogueira LM, Dunlap SM, Ford NA, Hursting SD. Calorie restriction and rapamycin inhibit MMTV-Wnt-1 mammary tumor growth in a mouse model of postmenopausal obesity. Endocr Relat Cancer 2012; 19:57-68. [PMID: 22143497 DOI: 10.1530/erc-11-0213] [Citation(s) in RCA: 56] [Impact Index Per Article: 4.3] [Reference Citation Analysis] [Abstract] [MESH Headings] [Grants] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 12/17/2022]
Abstract
Obesity is an established risk and progression factor for postmenopausal breast cancer. Interventions to decrease caloric intake and/or increase energy expenditure beneficially impact tumor progression in normoweight humans and animal models. However, despite the increasingly high global prevalence of obesity, the effects and underlying mechanisms of these energy balance modulating interventions are poorly characterized in obese individuals. The goal of this study was to better characterize the mechanism(s) responsible for the link between energy balance and breast cancer progression in the postmenopausal obesity context. We compared the effects of calorie restriction (CR), treadmill exercise (EX), and mammalian target of rapamycin (mTOR inhibitor) treatment on body composition, serum biomarkers, cellular signaling, and mammary tumor growth in obese mice. Ovariectomized C57BL/6 mice were administered a diet-induced obesity regimen for 8 weeks, then randomized into three treatment groups: control (semipurified diet fed ad libitum, maintained the obese state); 30% CR (isonutrient relative to control except 30% reduction in carbohydrate calories); and EX (control diet fed ad libitum plus treadmill exercise). Mice were implanted with syngeneic MMTV-Wnt-1 mammary tumor cells at week 12. Rapamycin treatment (5 mg/kg every 48 h) started at week 14. Tumors were excised at week 18. CR and rapamycin (but not EX) significantly reduced final tumor weight compared to control. In follow-up analysis, constitutive activation of mTOR ablated the inhibitory effects of CR on Wnt-1 mammary tumor growth. We conclude that mTOR inhibition may be a pharmacologic strategy to mimic the anticancer effects of CR and break the obesity-breast cancer progression link.
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Affiliation(s)
- Leticia M Nogueira
- Institute of Cell and Molecular Biology, University of Texas at Austin, Austin, Texas 78712, USA
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Luis-Rodríguez D, Martínez-Castelao A, Górriz JL, De-Álvaro F, Navarro-González JF. Pathophysiological role and therapeutic implications of inflammation in diabetic nephropathy. World J Diabetes 2012; 3:7-18. [PMID: 22253941 PMCID: PMC3258536 DOI: 10.4239/wjd.v3.i1.7] [Citation(s) in RCA: 93] [Impact Index Per Article: 7.2] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 08/26/2011] [Revised: 12/09/2011] [Accepted: 01/09/2012] [Indexed: 02/05/2023] Open
Abstract
Diabetes mellitus and its complications are becoming one of the most important health problems in the world. Diabetic nephropathy is now the main cause of end-stage renal disease. The mechanisms leading to the development and progression of renal injury are not well known. Therefore, it is very important to find new pathogenic pathways to provide opportunities for early diagnosis and targets for novel treatments. At the present time, we know that activation of innate immunity with development of a chronic low grade inflammatory response is a recognized factor in the pathogenesis of diabetic nephropathy. Numerous experimental and clinical studies have shown the participation of different inflammatory molecules and pathways in the pathophysiology of this complication.
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Affiliation(s)
- Desirée Luis-Rodríguez
- Desirée Luis-Rodríguez, Alberto Martínez-Castelao, José Luis Górriz, Fernando de Álvaro, Juan F Navarro-González, Grupo Español para el Estudio de la Nefropatía Diabética (GEENDIAB), Spain
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Ruscica M, Steffani L, Magni P. Adiponectin interactions in bone and cartilage biology and disease. VITAMINS AND HORMONES 2012; 90:321-39. [PMID: 23017721 DOI: 10.1016/b978-0-12-398313-8.00012-9] [Citation(s) in RCA: 11] [Impact Index Per Article: 0.8] [Reference Citation Analysis] [Abstract] [Track Full Text] [Subscribe] [Scholar Register] [Indexed: 12/27/2022]
Abstract
The adipokine adiponectin promotes insulin sensitivity and fat β-oxidation. In addition to its metabolic effects, adiponectin is an important local and systemic modulator of bone remodeling and cartilage biology, involving direct and indirect mechanisms and a large set of downstream molecular signals. Moreover, data suggest that changes in adiponectin signaling may be associated with bone and cartilage diseases. Adiponectin seems to exert a negative net effect on bone mass and to be an independent predictor of lower bone mass, whereas available data about actions on cartilage are more controversial, showing both pro- and anti-inflammatory actions. Adiponectin-bone cross talk seems to be reciprocal, as osteocalcin, produced by osteoblasts, has been shown to stimulate adiponectin expression and to improve glucose tolerance. Adiponectin-related signaling in bone and cartilage should be considered within the network of hormonal and nutritional signals that may influence skeleton biology, together with body homeostasis and adipose mass changes.
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Affiliation(s)
- Massimiliano Ruscica
- Department of Pharmacological and Biomolecular Sciences, Università degli Studi di Milano, Milan, Italy
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