Adiponectin: linking the metabolic syndrome to its cardiovascular consequences

Rabin, Karen R.; Kamari, Yehuda; Avni, Irit; Grossman, Ehud; Sharabi, Yehonatan

doi:10.1586/14779072.3.3.465

Cited by 44 publications

(34 citation statements)

References 75 publications

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“…There is strong evidence in the literature linking low levels of adiponectin with the development of the metabolic syndrome as well as with its consequences, type 2 diabetes and coronary artery disease (7,43). Adiponectin is even deemed a potential therapeutic agent (44). Animal models have shown that adiponectin is a potent insulin enhancer, regulating energy homeostasis and glucose tolerance (9 -11).…”

Section: Genetic Architecture Of Apm1 Genementioning

confidence: 99%

Genetic Architecture of the APM1 Gene and Its Influence on Adiponectin Plasma Levels and Parameters of the Metabolic Syndrome in 1,727 Healthy Caucasians

et al. 2006

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The associations of the adiponectin (APM1) gene with parameters of the metabolic syndrome are inconsistent. We performed a systematic investigation based on fine-mapped single nucleotide polymorphisms (SNPs) highlighting the genetic architecture and their role in modulating adiponectin plasma concentrations in a particularly healthy population of 1,727 Caucasians avoiding secondary effects from disease processes. Genotyping 53 SNPs (average spacing of 0.7 kb) in the APM1 gene region in 81 Caucasians revealed a two-block linkage disequilibrium (LD) structure and enabled comprehensive tag SNP selection. We found particularly strong associations with adiponectin concentrations for 11 of the 15 tag SNPs in the 1,727 subjects (five P values <0.0001). Haplotype analysis provided a thorough differentiation of adiponectin concentrations with 9 of 17 haplotypes showing significant associations (three P values <0.0001). No significant association was found for any SNP with the parameters of the metabolic syndrome. We observed a two-block LD structure of APM1 pointing toward at least two independent association signals, one including the promoter SNPs and a second spanning the relevant exons. Our data on a large number of healthy subjects suggest a clear modulation of adiponectin concentrations by variants of APM1, which are not merely a concomitant effect in the course of type 2 diabetes or coronary artery disease. Diabetes 55: [375][376][377][378][379][380][381][382][383][384] 2006

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Section: Genetic Architecture Of Apm1 Genementioning

confidence: 99%

Genetic Architecture of the APM1 Gene and Its Influence on Adiponectin Plasma Levels and Parameters of the Metabolic Syndrome in 1,727 Healthy Caucasians

et al. 2006

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“…1 Adiponectin levels are decreased in obesity, 2 and in cross-sectional studies an inverse association has been found between adiponectin and prevalent coronary heart disease (CHD). [3][4][5] Adiponectin is not the only adipose-tissue-derived protein that shows altered circulating levels in obesity with implications for CHD risk.…”

Section: Introductionmentioning

confidence: 99%

Differential association of adiponectin with cardiovascular risk markers in men and women? The KORA survey 2000

et al. 2006

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Background: In men, high adiponectin concentrations were related to a lower risk of myocardial infarction, whereas no association with cardiovascular events was found in women. Objective: To investigate sex differences in the associations of adiponectin with cardiovascular risk factors. Design: Cross-sectional population-based KORA Survey 2000 in Southern Germany using the same study methods for cardiovascular risk factors as the former WHO MONICA project. Participants: A total of 697 men and 657 women, aged 55-74 years. Glucose tolerance status was assessed by oral glucose tolerance tests. Results: Adiponectin (geometric mean, interquartile range; mg/ml) levels were significantly higher in women (11.1; 8.5-14.9) than in men (7.1; 5.2-9.6) (Po0.05). In univariate analyses, HDL-cholesterol and age were significantly positively correlated with adiponectin in both sexes. Negative correlations were observed with BMI, waist circumference, fasting and postchallenge glucose, insulin, HOMA-IR, HbA1c, triglycerides, uric acid and CRP (Po0.01). In sex-specific multivariate regression, age and HDL-cholesterol were independently positively, and fasting insulin and 2-h glucose were negatively related to adiponectin in both sexes. Uric acid was significantly inversely related to adiponectin in women only (sex interaction: P ¼ 0.02). Exploratory sex-specific factor analysis of adiponectin and the core components of the metabolic syndrome yielded four similar factors. Adiponectin loaded negatively on the 'lipids' factor in both sexes. Conclusion: The associations of adiponectin with cardiovascular risk factors showed a similar pattern in both sexes, except for uric acid. This small sex difference may not explain previous conflicting results on the association of adiponectin with cardiovascular events in men and women.

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“…Adiponectin (APN), an adipocytokine first described as the most abundant protein produced by adipocytes, appears to serve as a central regulatory protein in many of the physiological pathways controlling lipid and carbohydrate metabolism and to mediate various vascular processes. 1 APN displays both antiinflammatory and antiatherogenic properties, 2,3 and its levels are paradoxically decreased in obesity and insulin-resistance states including metabolic syndrome and diabetes, as well as hypertension and coronary artery disease. 4 APN interacts with two types of receptors, adipoR1 and adipoR2.…”

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confidence: 99%

Adiponectin-Mediated Heme Oxygenase-1 Induction Protects Against Iron-Induced Liver Injury via a PPARα-Dependent Mechanism

Lin

Jen

et al. 2010

The American Journal of Pathology

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Protective effects of adiponectin (APN; an adipocytokine) were shown against various oxidative challenges; however, its therapeutic implications and the mechanisms underlying hepatic iron overload remain unclear. Herein, we show that the deleterious effects of iron dextran on liver function and iron deposition were significantly reversed by adiponectin gene therapy, which was accompanied by AMP-activated protein kinase (AMPK) phosphorylation and heme oxygenase (HO)-1 induction. Furthermore, AMPK-mediated peroxisome proliferator-activated receptor-␣ (PPAR␣) activation by APN was ascribable to HO-1 induction. Additionally, we revealed direct transcriptional regulation of HO-1 by the binding of PPAR␣ to a PPAR-responsive element (PPRE) by various experimental assessments. Interestingly, overexpression of HO-1 in hepatocytes mimicked the protective effect of APN in attenuating iron-mediated injury, whereas it was abolished by SnPP and small interfering HO-1. Furthermore, bilirubin, the end-product of the HO-1 reaction, but not CO, protected hepatocytes from iron dextran-mediated caspase activation. Herein, we demonstrate a novel functional PPRE in the promoter regions of HO-1, and APN-mediated HO-1 induction elicited an antiapoptotic effect and a decrease in iron deposition in hepatocytes subjected to iron challenge.

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Adiponectin: linking the metabolic syndrome to its cardiovascular consequences

Cited by 44 publications

References 75 publications

Genetic Architecture of the APM1 Gene and Its Influence on Adiponectin Plasma Levels and Parameters of the Metabolic Syndrome in 1,727 Healthy Caucasians

Genetic Architecture of the APM1 Gene and Its Influence on Adiponectin Plasma Levels and Parameters of the Metabolic Syndrome in 1,727 Healthy Caucasians

Differential association of adiponectin with cardiovascular risk markers in men and women? The KORA survey 2000

Adiponectin-Mediated Heme Oxygenase-1 Induction Protects Against Iron-Induced Liver Injury via a PPARα-Dependent Mechanism

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