The role of Glutaredoxin-2 in the modulation of mitochondrial bioenergetics in female mice fed a high-fat diet

Abstract

Our group recently observed that male mice containing a deletion for the gene encoding the thiol oxidoreductase glutaredoxin-2 (GRX2) were protected from diet-induced obesity (DIO) and the development of related disorders (e.g. fatty liver disease). This effect was associated with increased fuel combustion in muscles. In the present study, I assessed if deleting the Grx2 gene protected female mice from DIO. Unlike male mice, in this study female wild-type (WT) littermates were completely resistant to developing DIO and related co-morbidities. Additionally, deletion of the Grx2 gene did not alter the weight gain profiles, adiposity, intrahepatic fatty acid and glycogen levels, or circulating triglycerides in these mice. Furthermore, while differences in reactive oxygen species generation in liver mitochondria were observed, this trend was not present in muscle mitochondria. Mitochondrial bioenergetics data revealed no differences in mitochondrial respiration between WT and GRX2-deficient female mice fed a control or high-fat diet.