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Moreover, it was recently reported that also in humans expression of adiponectin receptor in skeletal muscle is directly correlated with insulin sensitivity (16). The low electronic adiponectin levels in NAFLD patients reported in this study electronic may represent a pathogenic mechanism leading to altered hepatocyte lipid metabolism and fat accumulation. In fact, high adiponectin levels have been reported to protect against both electronic alcoholic and nonalcoholic fatty liver disease in mice by reducing fatty acid synthesis through inhibition of acyl-CoA carboxylase (ACC) and fatty acid synthase (FAS) expression and activity (8). The reduction of ACC activity reduces the malonyl-CoA level, which is known to inhibit carnitine palmitoyltransferase I (CPT-I) activity and fatty acid oxidation. Therefore, reduced adiponectin in NAFLD could result in increased fatty acid synthesis, accumulation of triglycerides, and reduced fatty acid oxidation.
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