Lower expression of adiponectin mRNA in visceral adipose tissue in lean and obese subjects

Lihn, Aina S.

doi:10.1016/s0303-7207(04)00098-x

Cited by 118 publications

(155 citation statements)

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“…41 In addition, peripheral adipose tissue expressed lower levels of inflammatory proteins, including 11-b-hydroxysteroid dehydrogenase-1, interleukin-6 and plasminogen activator inhibitor-1, compared with abdominal adipose tissue, and this may contribute to the protective effect of peripheral fat on insulin sensitivity. 42,43 Although the lowest tertile of PFM/CFM is associated with lower insulin sensitivity, we did not observe any significant differences between the other two groups, indicating that a threshold may exist. It may be that once the buffering capacity is reached, further increments of PFM do not improve the metabolic profile.…”

Section: Discussioncontrasting

confidence: 63%

Body fat distribution modulates insulin sensitivity in post-menopausal overweight and obese women: a MONET study

et al. 2008

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Objective: Central fat mass (CFM) correlates with insulin resistance and increases the risk of type 2 diabetes and cardiovascular complications. On the other hand, increased peripheral fat mass (PFM) is associated with higher insulin sensitivity. Thus, we examined the contribution of adipose tissue distribution, as assessed by the PFM/CFM ratio, to insulin sensitivity in overweight and obese postmenopausal women. Design and methods: A total of 124 nondiabetic overweight and obese postmenopausal women underwent an oral glucose tolerance test (OGTT) and a hyperinsulinemic/euglycemic (HI) clamp. Body composition was determined using computed tomography for visceral adipose tissue (VAT) and dual X-ray absorptiometry for fat mass, lean body mass and their respective proportions. Participants were divided by tertiles of the PFM/CFM ratio. Results: Participants with preferential CFM (group 1) had higher fasting insulin levels and insulin area under the curve (AUC) during OGTT, as well as lower glucose infusion rates during the HI clamp, whether it was expressed per kg of body weight (M) or per kg of fat-free mass (Mm), compared with the other two groups. The PFM/CFM ratio also correlated significantly with fasting insulin (r ¼ À0.32, Po0.001), the insulin AUC (r ¼ À0.42 Po0.001), M (r ¼ 0.39 Po0.001) and Mm (r ¼ 0.37 Po0.001). Using hierarchical regression, we demonstrated that the PFM/CFM ratio was an independent predictor of insulin AUC, M and Mm and that its sequential addition to CFM and VAT improved significantly the predictive value of the model for insulin sensitivity for all variables except fasting insulin. Conclusion: The PFM/CFM ratio, which integrates the antagonistic effects of both central and peripheral depots on insulin sensitivity, added substantially to the prediction of insulin sensitivity over VAT and CFM alone.

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Section: Discussioncontrasting

confidence: 63%

Body fat distribution modulates insulin sensitivity in post-menopausal overweight and obese women: a MONET study

et al. 2008

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“…Males [3] 19.373.9 Females [25] 35.8710.7 Triglycerides (mmol/l) [27] 1.971.4 Adiponectin (mg/ml) [21] 14.476.9…”

Section: Discussionmentioning

confidence: 99%

“…The absence of a difference between visceral and subcutaneous adiponectin mRNA levels in obese subjects is in line with a previous study which showed significantly lower APM1 mRNA levels in visceral compared to subcutaneous adipose tissue in lean subjects, but only a nonsignificant trend in obese subjects. 21 In humans, subcutaneous adiponectin mRNA levels are reduced in obesity, 29 independently of the degree of insulin resistance. 30 In obese type 2 diabetic subjects, both visceral and subcutaneous APM1 mRNA levels have been reported to be reduced.…”

Section: Discussionmentioning

confidence: 99%

“…14,19 Earlier studies have shown that APM1 expression is reduced in visceral compared to subcutaneous adipose tissue in normal-weight subjects. 21 However, adiponectin secretion was higher in cultured human omental adipocytes than in subcutaneous adipocytes. 22 Adiponectin serum levels have a heritability of about 30%, 18 indicating that genetic variation within or outside the adiponectin gene could affect the expression of the gene.…”

Section: Introductionmentioning

confidence: 97%

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A polymorphism in the adiponectin gene influences adiponectin expression levels in visceral fat in obese subjects

et al. 2005

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Objective: Reduced serum adiponectin levels have been found in obesity and type 2 diabetes and variations in the adiponectin gene (APM1) have been associated with type 2 diabetes and features of the metabolic syndrome in different populations. Study Design: Here, we investigated the expression of APM1 in adipose tissue and studied the relationship between variation in APM1 expression, the APM1 G276T polymorphism, the common PPARG Pro12Ala polymorphism and clinical features of 36 morbidly obese (body mass index (BMI) 41.574.9 kg/m 2 ) nondiabetic subjects. Results: APM1 mRNA expression in visceral fat was correlated with serum adiponectin levels (r ¼ 0.54, P ¼ 0.012). In visceral, but not in subcutaneous, adipose tissue APM1 mRNA level was 38% higher among carriers of the APM1 G276T T allele

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“…The average of triplicates from each sample was used. The relative quantification of target gene was calculated by the formula (½) Ct-target gene-Ct-housekeeping gene , which is described in the Users Bulletin 2, 1997, from Perkin-Elmer (Perkin-Elmer Cetus, Norwalk, CT, USA) [13].…”

Section: Methodsmentioning

confidence: 99%

Mannose-binding lectin deficiency attenuates renal changes in a streptozotocin-induced model of type 1 diabetes in mice

et al. 2007

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Aims/hypothesis An increasing amount of evidence indicates that mannose-binding lectin (MBL) plays a role in the development of diabetic nephropathy. The main objective of the study was to analyse whether MBL influences the effects of diabetes on the kidneys. Materials and methods In one group of wild-type mice and in one group of MBL double knockout mice we induced diabetes by the use of streptozotocin as a model of type 1 diabetes. Two groups of non-diabetic mice, wild-type and MBL knockout, were also included. By two-way ANOVA we evaluated if MBL modulated the effects of diabetes by testing the interaction between diabetes and MBL. Results MBL interacted with the effects of diabetes on three outcome measures: kidney weight (p<0.001), urinary albumin excretion (p=0.001) and the expression of collagen IVα1 (Col4a1) mRNA (p=0.002). This means that the effects that diabetes normally has on these parameters were significantly modified by MBL. MBL showed a tendency to interact with the effects of diabetes on glomerular basement membrane thickness and total mesangial volume (p=0.065 and p=0.063, respectively). Glomerular volume and total mesangial volume were significantly smaller in animals lacking MBL than in wild-type animals (p=0.006 and p=0.047, respectively). Conclusions/interpretation These findings, for the first time, show that the degree of kidney alteration as a consequence of diabetes is modified by MBL. These findings support a pivotal role of MBL in the development of diabetic kidney disease.

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Lower expression of adiponectin mRNA in visceral adipose tissue in lean and obese subjects

Cited by 118 publications

References 0 publications

Body fat distribution modulates insulin sensitivity in post-menopausal overweight and obese women: a MONET study

Body fat distribution modulates insulin sensitivity in post-menopausal overweight and obese women: a MONET study

A polymorphism in the adiponectin gene influences adiponectin expression levels in visceral fat in obese subjects

Mannose-binding lectin deficiency attenuates renal changes in a streptozotocin-induced model of type 1 diabetes in mice

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