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Adipocyte iron regulates adiponectin and insulin sensitivity. - PubMed - NCBI

Iron overload is associated with increased diabetes risk. We therefore investigated the effect of iron on adiponectin, an insulin-sensitizing adipokine that is decreased in diabetic patients. In humans, normal-range serum ferritin levels were inversely associated with adiponectin, independent of inflammation. Ferritin was increased and adiponectin was decreased in type 2 diabetic and in obese diabetic subjects compared with those in equally obese individuals without metabolic syndrome. Mice fed a high-iron diet and cultured adipocytes treated with iron exhibited decreased adiponectin mRNA and protein. We found that iron negatively regulated adiponectin transcription via FOXO1-mediated repression. Further, loss of the adipocyte iron export channel, ferroportin, in mice resulted in adipocyte iron loading, decreased adiponectin, and insulin resistance. Conversely, organismal iron overload and increased adipocyte ferroportin expression because of hemochromatosis are associated with decreased adipocyte iron, increased adiponectin, improved glucose tolerance, and increased insulin sensitivity. Phlebotomy of humans with impaired glucose tolerance and ferritin values in the highest quartile of normal increased adiponectin and improved glucose tolerance. These findings demonstrate a causal role for iron as a risk factor for metabolic syndrome and a role for adipocytes in modulating metabolism through adiponectin in response to iron stores.


Manganese supplementation increases adiponectin secretion by upregulating disulfide bond A-like protein in endothelial cells and Zucker diabetic fatty rats (767.13)

Adiponectin is an insulin sensitizer that plays a role in the regulation of lipid and glucose homeostasis and has anti atherosclerotic effects. It is synthesized as a single polypeptide and is then assembled in the endoplasmic reticulum into different multimers. An adiponectin-interacting protein named disulfide bond A-like protein (DsbA-L) was recently found to play an important role in multimerization of adiponectin; impairment in DsbA-L is associated with diabetes and low adiponectin levels. Manganese (Mn) levels have been found to be low in atherosclerotic and diabetic patients. Previous studies in our lab have shown that Mn supplementation can lower blood cholesterol and ICAM-1 levels in ZDF rats and reduce MCP-1 secretion and monocyte adhesion to endothelial cells in HUVECs model (J. Biol. Chem, 2013 Mar 1; 288 (9):6409-16). This study investigates the hypothesis that Mn supplementation affects DsbA-L expression levels, and thereby adiponectin levels, in ZDF rats and endothelial cells (HUVECs). Results show that diabetic rats supplemented with Mn (gavaged daily with 16 mg/kg BW for seven weeks, n=5) have higher plasma adiponectin levels (41%, p=0.007) and higher DsbA-L expression in the liver compared to control diabetic rats (n=6). Similarly, pre-treatment with Mn (with 5 or 10 μM for 24 h) prevented the decrease in DsbAL expression and adiponectin levels in HUVECs and 3T3L1 adipocyte cells exposed to high glucose and MCP-1. We further investigated the role of DsbA-L protein by knocking down its expression in HUVECs. Preliminary studies with DsbA-L siRNA show that beneficial effects of Mn supplementation on NOX4 expression and other biomarkers of vascular inflammation were abolished in DsbA-L knocked down cells. Thus, this study demonstrates that DsbA-L mediates the beneficial effects of Mn on adiponectin and provides a novel mechanism by which Mn supplementation reduces biomarkers of vascular inflammation in diabetes.

The Effect of Zinc Supplementation on Serum Adiponectin Concentration and Insulin Resistance in First Degree Relatives of Diabetic Patients - Iranian Journal of Diabetes and Obesity

Objective: Adiponectin (an insulin sensitizing protein) and zinc have insulin like effect. This study was conducted to assess the effect of zinc supplementation on serum adiponectin and insulin resistance in first degree relatives of diabetic patients.

Materials and Methods: This study was a randomized clinical trial performed on 58 first degree relatives of diabetic patients with normal glucose tolerance test and body mass index (BMI) more than 25Kg/m2. The subjects were divided into two groups: a case group which consumed 50mg zinc orally per day for twelve weeks and another group that was not given zinc but regular exercise and weight control were recommended. Adiponectin, fasting blood glucose, insulin and insulin resistance were calculated by the homeostasis model assessment (HOMA) and lipid profile was measured in both groups before and after treatment.

Results: The mean age and BMI of participants were 37.6±7.4 years and 28.8±3.5 Kg/m2 respectively. The level of adiponectin increased significantly from 1.67 ±1.29 to 3.67± 3.08 mIU/ml in subjects who received 50 mg zinc compared to the control group (p=0.001). HOMA decreased from 1.89±1.07 to 1.54±1.34 in subjects who consumed zinc, but this reduction was not significant (p=0.13).

Conclusion: Zinc significantly increases the level of adiponectin in first degree relatives of diabetic patients. The level of insulin and HOMA index after zinc supplementation decreased but this reduction was not significant.

Vitamin D: A New Player In Non-alcoholic Fatty Liver Disease?

Vaidya et al[40] showed a positive association between 25(OH)D concentrations and levels of adiponectin in a large cohort of patients

In murine models, high levels of adiponectin have been experimentally shown to decrease necroinflammation and steatosis in alcoholic and nonalcoholic fatty liver disease[36] as well as improved insulin resistance[37]. Moreover, studies in humans showing reduced serum levels of adiponectin and reduced hepatic expression of its receptor in patients with NASH compared with body mass index-matched patients with steatosis[38,39], provide strong supportive evidence that reduced adipocyte production of adiponectin plays an important role in the pathogenesis of progressive NAFLD.

Phototherapy also improved insulin resistance and increased serum adiponectin in association with reduced hepatic expression of inflammatory genes TNF-α and TFG-β. In total, these findings suggest that vitamin D deficiency worsens NAFLD related to upregulation of hepatic inflammatory and oxidative stress genes.
 
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