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This Article Accepted manuscript (PDF) All Versions of this Article: JOE-08-0026v1 199/1/95    most recent Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Feng, L. Articles by Zhao, J. Search for Related Content PubMed PubMed Citation Articles by Feng, L. Articles by Zhao, J.

L Feng, Endocrinology, Provincial Hospital affiliated to Shandong University, Jinan, China
L Gao, central laboratory, Provincial Hospital affiliated to Shandong University, Jinan, China
Q Guan, Endocrinology, Provincial Hospital affiliated to Shandong University, Jinan, China
X Hou, central laboratory, Provincial Hospital affiliated to Shandong University, Jinan, China
Q Wan, nephrology, Provincial Hospital affiliated to Shandong University, Jinan, China
X Wang, Shandong University School of Medicine, Jinan, China
J Zhao, Endocrinology, Provincial Hospital affiliated to Shandong University, Jinan, China

Correspondence: Jiajun Zhao, Email: jiajunzhao{at}163.com

Abstract

The sole effect of either saturated fatty acid or moderate ethanol consumption on GLUT4 expression is widely reported but the combined effects of them remain obscure. Here, we observed their combined effects on GLUT4 expression, explored the underlying mechanism mediated by AMP-activated protein kinase (AMPK ) and myocyte enhancer factor 2 (MEF2) both in vivo and in vitro. In the in vivo experiments, thirty-six male wistar rats, divided into three groups, were fed with normal diet, high-fat diet, or high-fat diet plus ethanol for 22 weeks. We measured expression of total-AMPK (T-AMPK ), phosphorylated-AMPK (pAMPK , activated form of AMPK), MEF2 and GLUT4 in epididymal adipose tissues. In the in vitro experiments, primary adipocytes, isolated from normal wistar rats, were incubated in the presence or absence of palmitate, ethanol, and compound C (an AMPK inhibitor) for 1h. Thereafter, T-AMPK , pAMPK , MEF2 and GLUT4 expression was measured. We found that both high-fat diet and in vitro exposition to palmitate impaired GLUT4 expression in rat adipocytes with a parallel reduction in AMPK activation and MEF2 expression. This impairment was reversed by ethanol administration. We further demonstrated that ethanol-mediated AMPK activation stimulates MEF2 and GLUT4 expression in adipocytes, as evidenced by compound C blockade of these effects. In summary, long-term moderate ethanol consumption reversed the adverse effect of saturated fatty acid on GLUT4 expression in adipocytes, which was likely to be a result from AMPK activation and subsequent upregulation of MEF2 and GLUT4 expression.