期刊
MOLECULAR AND CELLULAR ENDOCRINOLOGY
卷 358, 期 1, 页码 63-68出版社
ELSEVIER IRELAND LTD
DOI: 10.1016/j.mce.2012.02.022
关键词
Mouse; 3T3-L1; mTOR; Gene expression; Chromatin immunoprecipitation; C/EBP alpha
资金
- CIHR [MOP-66967, CCI-85677]
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 alpha (C/EBP alpha) to the IGFBP-2 proximal promoter. These findings suggest that insulin upregulates IGFBP-2 expression through a PI3K/mTOR/C/EBP alpha pathway in white adipocytes. (c) 2012 Elsevier Ireland Ltd. All rights reserved.
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