Figure 2.

Functions of the antioxidant enzyme systems in adipose tissues. In adipocytes, catalase inhibits lipogenesis and Nox4 expression, which prevents weight gain and fat mass increase induced by high-fat diet. Overexpression of catalase and superoxide dismutase (SOD)-1 in adipocytes can inhibit ectopic fat accumulation and improve insulin sensitivity. Heme oxygenase 1 (HO1) can stimulate the expression of adiponectin, therefore preventing hyperglycemia and insulinemia in female mice, and improving vascular function and insulin sensitivity. Peroxiredoxin (Prx)-2 can promote adipogenesis, whereas Prx3 can stimulate the expression of adiponectin. Depletion of these antioxidant enzymes in adipocytes has shown detrimental effects in adipocyte functions and promoted cardiometabolic diseases. Glutamate-cysteine ligase (Gclc) facilitates glutathione synthesis and inhibits ROS production, thereby inhibiting ectopic fat accumulation and insulin resistance. On the other hand, deletion of either SOD2 or glutathione peroxidases (GPx) has been reported to provide beneficial effect in adipose tissue function. The anti-obesity effect of SOD2 deletion in adipocytes can be attributed to an activated mitochondrial biogenesis and enhanced mitochondrial fatty acid oxidation, which can promote energy expenditure. Insulin signaling can be enhanced by knocking down GPx in either muscle cells and hepatocytes. GPx-1 deletion can attenuate inflammation and enhance browning in visceral adipose tissues.