NT-PGC-1α deficiency attenuates high-fat diet-induced obesity by modulating food intake, fecal fat excretion and intestinal fat absorption.

摘要: Transcriptional coactivator PGC-1α and its splice variant NT-PGC-1α regulate metabolic adaptation by modulating many gene programs. Selective ablation of attenuates diet-induced obesity through enhancing fatty acid oxidation thermogenesis upregulation in brown adipose tissue (BAT). Recently, we have shown that selective reduces BAT. Thus, the objective this study was to test our hypothesis NT-PGC-1α-/- mice would be more prone obesity. Male female NT-PGC-1α+/+ (WT) were fed a regular chow or 60% high-fat (HF) diet for 16 weeks. Contrary expectations, both male HFD protected from obesity, with pronounced effects females. This lean phenotype primarily driven reduced dietary fat intake. Intriguingly, HFD-fed female, but not male, further exhibited decreased feed efficiency, which closely associated increased fecal excretion uptake acids intestinal enterocytes adipocytes concomitant decrease transporter expression. Collectively, results highlight role regulating whole body lipid homeostasis under conditions.