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Overexpression of glutathione peroxidase‐1 induces steatosis in mouse (374.3)

Our laboratory has previously found insulin resistance and obesity in mice overexpressing Se‐dependent glutathione peroxidase‐1 (GPX1‐OE). The present study was conducted to determine if and how hepatic lipid metabolism was related to these metabolic phenotypes in the GPX1‐OE mice. Liver samples were collected from male GPX1‐OE and the wild‐type mice at ages of 3 wk and 2, 6, 9, and 12 mo (n = 5‐10, fed an Se‐adequate Torula yeast‐sucrose diet) to determine lipid profiles and the mRNA and protein levels of factors involved in triglyceride synthesis, lipid deposition, β‐oxidation, and lipid hydrolysis. The time‐course indicated that obesity was observed at 6 mo of age and was preceded by the development of insulin resistance in the GPX1‐OE mice. Steatosis was developed between 6 and 12 mo of age in these mice. Compared with the wild‐type, the GPX1‐OE mice showed up‐regulation (P < 0.05) of fatty acid synthase (FASN), carbohydrate response element‐binding protein (ChREBP), and sterol regulatory element‐binding proteins‐1c (SREBP1c) protein or enzyme activity. In contrast, these mice, starting from 6 mo of age, showed down‐regulations (P < 0.05) of peroxisome proliferator‐activated receptor beta (PPARβ), carnitine palmitoyltransferase I (CPT1α), and adipose triglyceride lipase (ATGL) protein or activity. In conclusion, overexpression of GPX1 induced steatosis in mice from 6 mo of age by stimulating the triglyceride synthesis pathway and inhibiting the fatty acid oxidation and lipid pathway. These findings imply that the GPX1‐OE mouse may be a novel model for studying steatohepatitis associated with obesity and diabetes.