Role of Kruppel-like factor 15 in PEPCK gene expression in the liver
Role of Kruppel-like factor 15 in PEPCK gene expression in the liver
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DOI：
10.1016/j.bbrc.2004.12.096
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发表时间：
2005-02-18
影响因子：
3.1
通讯作者：
Kasuga, M
中科院分区：
文献类型：
--
作者：
Teshigawara, K;Ogawa, W;Kasuga, M
肝脏基因表达的调节对于能量稳态是重要的。我们现在表明，肝脏的基因表达的转录因子Kruppel样因子15（KLF 15）增加了食物剥夺和减少喂养小鼠。KLF 15基因在小鼠肝脏中的表达也被正血糖-高胰岛素钳夹下调，并通过抑制磷脂酰肌醇3-激酶而增加。在培养的大鼠肝细胞中，KLF 15基因的表达诱导地塞米松和非水解类似物的cAMP，这种效果被抑制胰岛素的方式依赖于磷脂酰肌醇3-激酶信号。在培养的肝细胞中强制表达KLF 15增加了磷酸烯醇丙酮酸羧激酶（PEPCK）基因的表达和启动子活性。这些结果表明，胰岛素及其抵消激素调节KLF 15的肝脏表达，并且该转录因子有助于肝脏中PEPCK基因表达的调节。(C)2004年爱思唯尔公司All rights reserved.
Regulation of hepatic gene expression is important for energy homeostasis. We now show that hepatic expression of the gene for the transcription factor Kruppel-like factor 15 (KLF15) is increased by food deprivation and reduced by feeding in mice. Expression of the KLF15 gene in mouse liver was also down-regulated by a euglycemic-hyperinsulinemic clamp and was increased by inhibition of phosphatidylinositol 3-kinase. In cultured rat hepatocytes, KLF15 gene expression was induced by dexamethasone and a non-hydrolyzing analog of cAMP, and this effect was inhibited by insulin in a manner dependent on phosphatidylinositol 3-kinase signaling. Forced expression of KLF15 in cultured hepatocytes increased both the expression and the promoter activity of the gene for phosphoenolpyruvate carboxykinase (PEPCK). These results suggest that insulin and its counteracting hormones regulate the hepatic expression of KLF15, and that this transcription factor contributes to the regulation of PEPCK gene expression in the liver. (C) 2004 Elsevier Inc. All rights reserved.