Differences in Adiponectin Protein Expression: Effect of Fat Depots and Type 2 Diabetic Status

Fisher, Ffolliott M.; McTernan, P. G.; Valsamakis, Georgios; Chetty, R.; Harte, A. L.; Anwar, Arif; Starcynski, Jane; Crocker, John F. S.; Barnett, Anthony; McTernan, Claire L.; Kumar, Sudhesh

doi:10.1055/s-2002-38246

Cited by 123 publications

(91 citation statements)

References 21 publications

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“…10,11 However, the data in type 2 diabetic patients are conflicting. 19,34,39,40 Our results, while confirming lower expression and plasma concentrations in association with obesity, do not show an independent effect of hyperglycemia, in agreement with Koistinen et al 40 On the other hand, our diabetic subjects were all severely obese, so that expression and circulating levels may have bottomed out (a 'floor effect'). Therefore, we cannot completely rule out that hyperglycemia in non-obese (or less obese) subjects may be associated with suppressed ApN.…”

Section: Discussionsupporting

confidence: 90%

Pattern of expression of adiponectin receptors in human adipose tissue depots and its relation to the metabolic state

et al. 2007

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Objective: To investigate whether adiponectin receptor genes (AdipoR1 and AdipoR2) expression in human subcutaneous (SAT) and visceral (VAT) adipose tissue in severely obese patients with or without diabetes is related to adiponectin gene (APM1) expression and in vivo metabolic parameters. Design: Cross-sectional, clinical research study. Subjects: Total RNA was extracted from SAT and VAT tissue obtained during surgery from 13 lean controls, 30 obese diabetic patients, 19 obese glucose-intolerant patients and 54 obese subjects with normal glucose tolerance. Measurements: Tissue expression of APM1, AdipoR1 and AdipoR2, tissue concentration of adiponectin (ApN), and metabolic variables. Results: APM1 expression was higher in SAT than VAT (1.0670.76 vs 0.6970.52, Po0.0001) as was AdipoR1 (1.1770.70 vs 0.6670.38, Po0.0001) and AdipoR2 (7.0276.19 vs 0.7570.64, Po0.0001). In SAT, APM1 and AdipoR1 expression tended to be lower -by 0.3870.22 and 0.3570.22, respectively -and AdipoR2 expression was markedly depressed -by 4.8271.93 -in association with obesity, whereas presence of diabetes had no additional effect. In VAT, APM1 and AdipoR1 expressions were also reduced -by 0.3670.16 and 0.3070.11, respectively -in association with obesity. Within both SAT and VAT, expression levels of APM1, AdipoR1 and AdipoR2 were all positively interrelated. Tissue ApN concentrations in SAT were similar across groups, whereas ApN levels in VAT were substantially lower in association with obesity (by an average of 63712 ng/mg total protein, Po0.0001). In multivariate models adjusting for sex, age and obesity, serum triglyceride concentrations were reciprocally related to APM1 (r ¼ À0.27, Po0.02), AdipoR1 (r ¼ À0.37, Po0.002 and AdipoR2 expression (r ¼ À0.37, Po0.002) in VAT. Likewise, plasma insulin concentrations were inversely related only to APM1 in VAT (r ¼ À0.25, Po0.03). Conclusions: Severe obesity is associated with suppressed expression of both ApN and its receptors in both SAT and VAT, the expression levels in VAT are specifically linked with hyperinsulinemia and dyslipidemia.

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Section: Discussionsupporting

confidence: 90%

Pattern of expression of adiponectin receptors in human adipose tissue depots and its relation to the metabolic state

et al. 2007

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“…23 Similar to the reported differences in adiponectin expression 17,18 and estradiol formation, 14,16 insulin responsiveness also appears to be different between subcutaneous and visceral adipocytes of nondiabetic obese subjects; the latter showing decreased responsiveness attributable to reduced insulin receptor autophosphorylation and reduced expression and tyrosine phosphorylation of insulin receptor substrate 1 (IRS-1). 24 Prolonged exposure of adipocytes to increased plasma estradiol, for example, during pregnancy 25 or in women with central obesity, 26,27 appears to be to prone to decreased IRS-1 expression.…”

Section: Discussionmentioning

confidence: 56%

“…In further support, subcutaneous adipocytes (both abdominal and gluteal) of nondiabetic obese subjects were shown to have maintained high adiponectin expression/secretion compared with the low expression/secretion of visceral adipocytes. 17,18 In diabetic subjects, adiponectin expression/secretion of subcutaneous adipocytes is also low, 18 suggesting that hormonal milieu characteristics for insulin-resistant/centrally obese subjects may inhibit adiponectin in both fat depots. Hormonal changes characteristic for centrally obese women versus generally and peripherally obese women included markedly decreased SHBG and increased estradiol levels.…”

Section: Discussionmentioning

confidence: 99%

Novel Associations Between Bioavailable Estradiol and Adipokines in Elderly Women With Different Phenotypes of Obesity

et al. 2004

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Background-Peripheral adiposity confers protection against diabetes and atherosclerosis in elderly women. The underlying mechanisms, however, remain to be elucidated. Methods and Results-On the basis on dual-energy X-ray absorptiometry measurements of central fat mass (CFM) and peripheral fat mass (PFM), we identified 290 elderly women with distinct forms of body fat distribution (lean, peripheral obesity, central obesity, or general obesity). Study parameters were plasma tumor necrosis factor-␣, interleukin (IL)-6, adiponectin, estradiol, sex hormone-binding globulin, insulin resistance, and aortic calcification, graded on lateral radiography. In peripherally and generally obese women, plasma estradiol and insulin resistance were significantly lower, whereas sex hormone-binding globulin and adiponectin were significantly higher compared with centrally obese women independent of age, body mass index, total fat mass, and smoking habits (all PϽ0.05). After adjustment for these confounders, IL-6 in centrally obese women was comparable with that seen in generally obese (similar high CFM%) but significantly higher than in peripherally obese women and lean women (low CFM%). Atherosclerosis was less severe in generally obese (2.5Ϯ0.3) compared with centrally obese women (5.0Ϯ0.7, Pϭ0.001). In multiple regression analysis, total fat mass, body fat distribution, insulin resistance, estradiol, current smoking, treated hyperlipidemia, and treated hypertension contributed independently to the variation of aortic calcification (Rϭ0.55, SEEϭ3.60, PϽ0.001). Conclusions-Abundant presence of PFM in generally obese women is associated with increased plasma adiponectin and higher insulin sensitivity, which could explain the apparent protection against the atherogenic effects of IL-6 derived from CFM. Low peripheral exposure to estradiol appears to be a sine qua non of maintained adiponectin secretion from

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“…16,93 There is a negative association between adiponectin and waist-to-hip ratio, central fat mass accumulation and visceral fat mass. 6,88,[94][95][96][97] Further, in vitro studies have shown that adiponectin protein content and mRNA expression are lower in visceral adipocytes 98 and that with increasing visceral fat mass adiponectin secretion from those cells is decreased, whereas secretion rates from subcutaneous adipocytes remain unaffected. 99 There is also a differential expression pattern of adiponectin receptor 1 with high levels of expression in subcutaneous fat.…”

Section: Adiponectinmentioning

confidence: 99%

Gluteofemoral body fat as a determinant of metabolic health

2010

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Body fat distribution is an important metabolic and cardiovascular risk factor, because the proportion of abdominal to gluteofemoral body fat correlates with obesity-associated diseases and mortality. Here, we review the evidence and possible mechanisms that support a specific protective role of gluteofemoral body fat. Population studies show that an increased gluteofemoral fat mass is independently associated with a protective lipid and glucose profile, as well as a decrease in cardiovascular and metabolic risk. Studies of adipose tissue physiology in vitro and in vivo confirm distinct properties of the gluteofemoral fat depot with regards to lipolysis and fatty acid uptake: in day-to-day metabolism it appears to be more passive than the abdominal depot and it exerts its protective properties by long-term fatty acid storage. Further, a beneficial adipokine profile is associated with gluteofemoral fat. Leptin and adiponectin levels are positively associated with gluteofemoral fat while the level of inflammatory cytokines is negatively associated. Finally, loss of gluteofemoral fat, as observed in Cushing's syndrome and lipodystrophy is associated with an increased metabolic and cardiovascular risk. This underlines gluteofemoral fat's role as a determinant of health by the long-term entrapment of excess fatty acids, thus protecting from the adverse effects associated with ectopic fat deposition.

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Differences in Adiponectin Protein Expression: Effect of Fat Depots and Type 2 Diabetic Status

Cited by 123 publications

References 21 publications

Pattern of expression of adiponectin receptors in human adipose tissue depots and its relation to the metabolic state

Pattern of expression of adiponectin receptors in human adipose tissue depots and its relation to the metabolic state

Novel Associations Between Bioavailable Estradiol and Adipokines in Elderly Women With Different Phenotypes of Obesity

Gluteofemoral body fat as a determinant of metabolic health

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