| First Author | Sisler JD | Year | 2015 |
| Journal | PLoS One | Volume | 10 |
| Issue | 12 | Pages | e0144444 |
| PubMed ID | 26689548 | Mgi Jnum | J:244129 |
| Mgi Id | MGI:5912908 | Doi | 10.1371/journal.pone.0144444 |
| Citation | Sisler JD, et al. (2015) The Signal Transducer and Activator of Transcription 1 (STAT1) Inhibits Mitochondrial Biogenesis in Liver and Fatty Acid Oxidation in Adipocytes. PLoS One 10(12):e0144444 |
| abstractText | The transcription factor STAT1 plays a central role in orchestrating responses to various pathogens by activating the transcription of nuclear-encoded genes that mediate the antiviral, the antigrowth, and immune surveillance effects of interferons and other cytokines. In addition to regulating gene expression, we report that STAT1-/- mice display increased energy expenditure and paradoxically decreased release of triglycerides from white adipose tissue (WAT). Liver mitochondria from STAT1-/- mice show both defects in coupling of the electron transport chain (ETC) and increased numbers of mitochondria. Consistent with elevated numbers of mitochondria, STAT1-/- mice expressed increased amounts of PGC1alpha, a master regulator of mitochondrial biogenesis. STAT1 binds to the PGC1alpha promoter in fed mice but not in fasted animals, suggesting that STAT1 inhibited transcription of PGC1alpha. Since STAT1-/- mice utilized more lipids we examined white adipose tissue (WAT) stores. Contrary to expectations, fasted STAT1-/- mice did not lose lipid from WAT. beta-adrenergic stimulation of glycerol release from isolated STAT1-/- WAT was decreased, while activation of hormone sensitive lipase was not changed. These findings suggest that STAT1-/- adipose tissue does not release glycerol and that free fatty acids (FFA) re-esterify back to triglycerides, thus maintaining fat mass in fasted STAT1-/- mice. |
