Published online May 18, 2015. doi: 10.4254/wjh.v7.i8.1012
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: 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.