Insulin stimulates IGFBP-2 expression in 3T3-L1 adipocytes through the PI3K/mTOR pathway

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• 作者：Zhuo Li^a ; ¹ ; Sté ; phanie Miard^a ; Mathieu Laplante^a ; Nahum Sonenberg^b ; Fré ; dé ; ric Picard^a ; ^{Frederic.Picard@criucpq.ulaval.ca}
• 关键词：Mouse ; 3T3-L1 ; mTOR ; Gene expression ; Chromatin immunoprecipitation ; C/EBP伪
• 刊名：Molecular and Cellular Endocrinology
• 出版年：2012
• 期刊代码：109_03037207
• 类别：bio
• 出版时间：6 July, 2012
• 卷：358
• 期：1
• 页码：63-68
• 文件大小：379 K

摘要

Insulin-like growth factor binding protein 2 (IGFBP-2) has been implicated in the etiology of several diseases, including the metabolic syndrome. Although IGFBP-2 derives mostly from the liver, recent evidence in mice and humans indicate that aging and obesity are associated with altered IGFBP-2 levels in white adipocytes. The present study was aimed at determining the mechanisms that control IGFBP-2 expression in mature adipocytes. IGFBP-2 mRNA and protein expression in serum-deprived 3T3-L1 adipocytes were twofold increased by acute insulin treatment. Co-treatments with the phosphatidylinositol 3-kinase (PI3K) inhibitor wortmannin or the mammalian target of rapamycin (mTOR) inhibitor rapamycin blunted the effects of insulin. Coherently, IGFBP-2 mRNA levels were robustly increased in adipocytes lacking either TSC2 or 4E-BP1. Insulin triggered the recruitment of CAAT/enhancer binding protein 伪 (C/EBP伪) to the IGFBP-2 proximal promoter. These findings suggest that insulin upregulates IGFBP-2 expression through a PI3K/mTOR/C/EBP伪 pathway in white adipocytes.