Author: ["Hiroshi Inoue","Wataru Ogawa","Michitaka Ozaki","Sanae Haga","Michihiro Matsumoto","Kensuke Furukawa","Naoko Hashimoto","Yoshiaki Kido","Toshiyuki Mori","Hiroshi Sakaue","Kiyoshi Teshigawara","Shiyu Jin","Haruhisa Iguchi","Ryuji Hiramatsu","Derek LeRoith","Kiyoshi Takeda","Shizuo Akira","Masato Kasuga"]
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Abstract
The transcription factor, signal transducer and activator of transcription-3 (STAT-3) contributes to various physiological processes. Here we show that mice with liver-specific deficiency in STAT-3, achieved using the Cre-loxP system, show insulin resistance associated with increased hepatic expression of gluconeogenic genes. Restoration of hepatic STAT-3 expression in these mice, using adenovirus-mediated gene transfer, corrected the metabolic abnormalities and the alterations in hepatic expression of gluconeogenic genes. Overexpression of STAT-3 in cultured hepatocytes inhibited gluconeogenic gene expression independently of peroxisome proliferator-activated receptor-γ coactivator-1α (PGC-1α), an upstream regulator of gluconeogenic genes. Liver-specific expression of a constitutively active form of STAT-3, achieved by infection with an adenovirus vector, markedly reduced blood glucose, plasma insulin concentrations and hepatic gluconeogenic gene expression in diabetic mice. Hepatic STAT-3 signaling is thus essential for normal glucose homeostasis and may provide new therapeutic targets for diabetes mellitus.Cite this article
Inoue, H., Ogawa, W., Ozaki, M. et al. Role of STAT-3 in regulation of hepatic gluconeogenic genes and carbohydrate metabolism in vivo. Nat Med 10, 168–174 (2004). https://doi.org/10.1038/nm980 