Editorial
Copyright ©The Author(s) 2016. Published by Baishideng Publishing Group Inc. All rights reserved.
World J Gastrointest Pathophysiol. Feb 15, 2016; 7(1): 17-26
Published online Feb 15, 2016. doi: 10.4291/wjgp.v7.i1.17
Adipose tissue-liver axis in alcoholic liver disease
Zhi-Gang Wang, Xiao-Bing Dou, Zhan-Xiang Zhou, Zhen-Yuan Song
Zhi-Gang Wang, College of Medical Laboratory Science and Technology, Harbin Medical University at Daqing, Daqing 163319, Heilongjiang Province, China
Xiao-Bing Dou, Zhen-Yuan Song, College of Life Science, Zhejiang Chinese Medical University, Hangzhou 310053, Zhejiang Province, China
Zhan-Xiang Zhou, Department of Nutrition, Center for Translational Biomedical Research, University of North Carolina at Greensboro, Kannapolis, NC 28081, United States
Zhen-Yuan Song, Department of Pathology, University of Illinois, Medical Center, Chicago, IL 60612, United States
Zhen-Yuan Song, Department of Kinesiology and Nutrition, University of Illinois at Chicago, Chicago, IL 60612, United States
Author contributions: All authors contributed to this paper.
Supported by National Institutes of Health NIAAA, No. R01 AA017442.
Conflict-of-interest statement: The authors declare no conflict of interest.
Open-Access: This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/
Correspondence to: Zhen-Yuan Song, PhD, Associate Professor, Department of Kinesiology and Nutrition, University of Illinois at Chicago, 1919 W Taylor Street, RM 627, Chicago, IL 60612, United States. song2008@uic.edu
Telephone: +1-312-9967892 Fax: +1-312-4130319
Received: May 26, 2015
Peer-review started: May 28, 2015
First decision: August 25, 2015
Revised: October 28, 2015
Accepted: November 24, 2015
Article in press: November 25, 2015
Published online: February 15, 2016
Processing time: 249 Days and 17.4 Hours
Abstract

Alcoholic liver disease (ALD) remains an important health problem worldwide. The disease spectrum is featured by early steatosis, steatohepatitis (steatosis with inflammatory cells infiltration and necrosis), with some individuals ultimately progressing to fibrosis/cirrhosis. Although the disease progression is well characterized, no effective therapies are currently available for the treatment in humans. The mechanisms underlying the initiation and progression of ALD are multifactorial and complex. Emerging evidence supports that adipose tissue dysfunction contributes to the pathogenesis of ALD. In the first part of this review, we discuss the mechanisms whereby chronic alcohol exposure contributed to adipose tissue dysfunction, including cell death, inflammation and insulin resistance. It has been long known that aberrant hepatic methionine metabolism is a major metabolic abnormality induced by chronic alcohol exposure and plays an etiological role in the pathogenesis of ALD. The recent studies in our group documented the similar metabolic effect of chronic alcohol drinking on methionine in adipose tissue. In the second part of this review, we also briefly discuss the recent research progress in the field with a focus on how abnormal methionine metabolism in adipose tissue contributes to adipose tissue dysfunction and liver damage.

Keywords: Alcohol; Lipolysis; Adipose; Methylation; Methionine; Liver

Core tip: Alcoholic liver disease (ALD) remains an important health problem worldwide. The disease spectrum is featured by early steatosis, steatohepatitis (steatosis with inflammatory cells infiltration and necrosis), with some individuals ultimately progressing to fibrosis/cirrhosis. Although the disease progression is well characterized, no effective therapies are currently available for the treatment in humans. The mechanisms underlying the initiation and progression of ALD are multifactorial and complex. Emerging evidence supports that adipose tissue dysfunction contributes to the pathogenesis of ALD. In this review, we discuss the mechanisms whereby chronic alcohol exposure contributed to adipose tissue dysfunction, as well as their contribution to ALD.