Role of Hepatic STAT3 in the Regulation of Lipid Metabolism

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Regulation of hepatic gene expression is largely responsible for the control ofnutrient metabolism. We previously showed that the transcription factor STAT3regulates glucose homeostasis by suppressing the expression of gluconeogenic genes inthe liver. However, the role of STAT3 in the control of lipid metabolism has remainedunknown. We have now investigated the effects of hepatic overexpression of STAT3,achieved by adenovirus-mediated gene transfer, on glucose and lipid metabolism ininsulin-resistant diabetic mice. Forced expression of STAT3 reduced blood glucose andplasma insulin concentrations as well as the hepatic abundance of mRNA forphosphoenolpyruvate carboxykinase. However, it also increased the plasma levels oftriglyceride and total cholesterol without affecting those of low density lipoprotein– orhigh density lipoprotein–cholesterol. The hepatic abundance of mRNAs for fatty acidsynthase and acetyl-CoA carboxylase, both of which catalyze the synthesis of fatty acids,was increased by overexpression of STAT3, whereas that of mRNAs for sterolregulatory element–binding proteins 1a, 1c, or 2 was unaffected. Moreover, the amountof mRNA for acyl-CoA oxidase, which contributes to β-oxidation, was decreased byforced expression of STAT3. These results indicate that forced activation of STAT3signaling in the liver of insulin-resistant diabetic mice increased the circulating levels ofatherogenic lipids through changes in the hepatic expression of genes involved in lipidmetabolism. Furthermore, these alterations in hepatic gene expression likely occurredthrough a mechanism independent of sterol regulatory element–binding proteins.
神戸大学の論文

Role of Hepatic STAT3 in the Regulation of Lipid Metabolism

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