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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 PGC1α, a master regulator of mitochondrial biogenesis. STAT1 binds to the PGC1α promoter in fed mice but not in fasted animals, suggesting that STAT1 inhibited transcription of PGC1α. 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. β-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.

The Signal Transducer and Activator of Transcription 1 (STAT1) Inhibits Mitochondrial Biogenesis in Liver and Fatty Acid Oxidation in Adipocytes