HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text Full Text (PDF) All Versions of this Article: 295/4/G833    most recent ajpgi.90358.2008v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Web of Science (8) Citing Articles via Google Scholar Google Scholar Articles by Ajmo, J. M. Articles by You, M. Search for Related Content PubMed PubMed Citation Articles by Ajmo, J. M. Articles by You, M.

LIVER AND BILIARY TRACT

Resveratrol alleviates alcoholic fatty liver in mice

Departments of Molecular Pharmacology and Physiology, University of South Florida Health Sciences Center, Tampa, Florida

Submitted 29 May 2008 ; accepted in final form 20 August 2008

Alcoholic fatty liver is associated with inhibition of sirtuin 1 (SIRT1) and AMP-activated kinase (AMPK), two critical signaling molecules regulating the pathways of hepatic lipid metabolism in animals. Resveratrol, a dietary polyphenol, has been identified as a potent activator for both SIRT1 and AMPK. In the present study, we have carried out in vivo animal experiments that test the ability of resveratrol to reverse the inhibitory effects of chronic ethanol feeding on hepatic SIRT1-AMPK signaling system and to prevent the development of alcoholic liver steatosis. Resveratrol treatment increased SIRT1 expression levels and stimulated AMPK activity in livers of ethanol-fed mice. The resveratrol-mediated increase in activities of SIRT1 and AMPK was associated with suppression of sterol regulatory element binding protein 1 (SREBP-1) and activation of peroxisome proliferator-activated receptor coactivator (PGC-1). In parallel, in ethanol-fed mice, resveratrol administration markedly increased circulating adiponectin levels and enhanced mRNA expression of hepatic adiponectin receptors (AdipoR1/R2). In conclusion, resveratrol treatment led to reduced lipid synthesis and increased rates of fatty acid oxidation and prevented alcoholic liver steatosis. The protective action of resveratrol is in whole or in part mediated through the upregulation of a SIRT1-AMPK signaling system in the livers of ethanol-fed mice. Our study suggests that resveratrol may serve as a promising agent for preventing or treating human alcoholic fatty liver disease.

alcoholic liver steatosis; lipid metabolism; sirtuin 1; AMP-activated kinase; acetylation; sterol regulatory element-binding protein 1c; peroxisome proliferator-activated receptor coactivator

This article has been cited by other articles:

				M. You and C. Q. Rogers Adiponectin: A Key Adipokine in Alcoholic Fatty Liver Experimental Biology and Medicine, August 1, 2009; 234(8): 850 - 859. [Abstract] [Full Text] [PDF]

				Z. Shen, J. M. Ajmo, C. Q. Rogers, X. Liang, L. Le, M. M. Murr, Y. Peng, and M. You Role of SIRT1 in regulation of LPS- or two ethanol metabolites-induced TNF-{alpha} production in cultured macrophage cell lines Am J Physiol Gastrointest Liver Physiol, May 1, 2009; 296(5): G1047 - G1053. [Abstract] [Full Text] [PDF]