Copyright ©The Author(s) 2015. Published by Baishideng Publishing Group Inc. All rights reserved.
World J Hepatol. May 18, 2015; 7(8): 1012-1019
Published online May 18, 2015. doi: 10.4254/wjh.v7.i8.1012
Peroxisome proliferator-activated receptors as targets to treat non-alcoholic fatty liver disease
Vanessa Souza-Mello
Vanessa Souza-Mello, Biomedical Centre, Institute of Biology, Department of Anatomy, State University of Rio de Janeiro, Rio de Janeiro 20551-030, Brazil
Author contributions: Souza-Mello V solely contributed to this paper.
Conflict-of-interest: The author discloses any 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: Vanessa Souza-Mello, RD, PhD, Biomedical Centre, Institute of Biology, Department of Anatomy, State University of Rio de Janeiro, Av. 28 de Setembro 87, Fundos, Vila Isabel, Rio de Janeiro 20551-030, Brazil. souzamello.uerj@gmail.com
Telephone: +55-21-28688689 Fax: +55-21-28688033
Received: January 27, 2015
Peer-review started: January 28, 2015
First decision: February 7, 2015
Revised: February 21, 2015
Accepted: March 30, 2015
Article in press: April 2, 2015
Published online: May 18, 2015
Core Tip

Core tip: Multiple pathways disrupted in obesity and non-alcoholic fatty liver disease (NAFLD) are regulated by genes encoded by peroxisome proliferator-activated receptors (PPARs). Thus, PPARs emerged as potential targets to alleviate NAFLD. The use of PPAR-alpha agonist yields increased mitochondrial beta-oxidation coupled with reduced lipogenesis. Both of them are essential to tackle insulin resistance and hepatic steatosis. PPAR-beta/delta agonist is still not available as a medicine, but PPAR-beta/delta agonist elicited expressive reduction in hepatic glucose production in murine models. PPAR-gamma agonist is extensively used, and beneficial effects come from partial activation as total PPAR-gamma activation leads to hepatic lipogenesis, being harmful to the liver.