| First Author | Kim J | Year | 2021 |
| Journal | Sci Rep | Volume | 11 |
| Issue | 1 | Pages | 1323 |
| PubMed ID | 33446719 | Mgi Jnum | J:300441 |
| Mgi Id | MGI:6502246 | Doi | 10.1038/s41598-020-79823-9 |
| Citation | Kim J, et al. (2021) NT-PGC-1alpha deficiency attenuates high-fat diet-induced obesity by modulating food intake, fecal fat excretion and intestinal fat absorption. Sci Rep 11(1):1323 |
| abstractText | Transcriptional coactivator PGC-1alpha and its splice variant NT-PGC-1alpha regulate metabolic adaptation by modulating many gene programs. Selective ablation of PGC-1alpha attenuates diet-induced obesity through enhancing fatty acid oxidation and thermogenesis by upregulation of NT-PGC-1alpha in brown adipose tissue (BAT). Recently, we have shown that selective ablation of NT-PGC-1alpha reduces fatty acid oxidation in BAT. Thus, the objective of this study was to test our hypothesis that NT-PGC-1alpha(-/-) mice would be more prone to diet-induced obesity. Male and female NT-PGC-1alpha(+/+) (WT) and NT-PGC-1alpha(-/-) mice were fed a regular chow or 60% high-fat (HF) diet for 16 weeks. Contrary to our expectations, both male and female NT-PGC-1alpha(-/-) mice fed HFD were protected from diet-induced obesity, with more pronounced effects in females. This lean phenotype was primarily driven by reduced dietary fat intake. Intriguingly, HFD-fed female, but not male, NT-PGC-1alpha(-/-) mice further exhibited decreased feed efficiency, which was closely associated with increased fecal fat excretion and decreased uptake of fatty acids by the intestinal enterocytes and adipocytes with a concomitant decrease in fatty acid transporter gene expression. Collectively, our results highlight the role for NT-PGC-1alpha in regulating whole body lipid homeostasis under HFD conditions. |
