Peroxiredoxin 6 Is a Key Antioxidant Enzyme in Modulating the Link between Glycemic and Lipogenic Metabolism

摘要: Insulin action and often glucose-stimulated insulin secretion are reduced in obesity. In addition, the excessive intake of lipids increases oxidative stress leading to overt type 2 diabetes mellitus (T2DM). Among antioxidative defense systems, peroxiredoxin 6 (PRDX6) is able reduce H2O2 short chain phospholipid hydroperoxides. Increasing evidences suggest that PRDX6 involved pathogenesis atherosclerosis T2DM, but its role etiopathology obesity complications still not known. Therefore, present study, we sought investigate this association by using knockout mice (PRDX6-/-). Metabolic parameters, like carbon dioxide (VCO2) production, oxygen consumption (VO2), respiratory exchange ratio (RER), were determined metabolic cages. Intraperitoneal glucose tolerance tests performed evaluate sensitivity tolerance, respectively. Liver pancreas histochemical analyses also evaluated. The expression enzymes lipid metabolism was analyzed real-time PCR. Following 24 weeks high-fat-diet (HFD), PRDX6-/- showed weight gain higher food drink compared controls. VO2 VCO2 production decreased mice, while RER lower than 0.7 indicating a prevalent metabolism. fed with HFD further deterioration on secretion. Furthermore, did suppress adipose tissue lipolysis consequent hepatic overload serum levels ALT, cholesterol, triglycerides. Interestingly, liver associated proinflammatory gene upregulation. Finally, rate nonalcoholic steatohepatitis (NASH) control. Our results may have functional protective development obesity-related disorders such as diseases T2DM be considered potential therapeutic target against these illnesses.