[PPAR and NASH]

Nihon Rinsho. 2006 Jun;64(6):1089-94.
[Article in Japanese]

Abstract

The nuclear receptor peroxisome proliferator-activated receptor (PPAR) plays important roles in maintaining the homeostasis of lipids and glucose. Among three isoforms of PPAR, PPARa and PPARgamma are localized mainly in hepatocytes and adipocytes, respectively. Recently, it has been recognized that PPAR also modulates inflammatory responses, regulates cell division and associates with liver fibrogenesis and tumorigenesis. Although the roles of PPAR for the pathogenesis of nonalcoholic steatohepatitis (NASH) remain unclear, several data suggest the relationship between PPAR and the occurrence or progression of NASH. For example, in mice lacking acyl-CoA oxidase gene, which developed NASH spontaneously, the absence of PPARalpha prevented the development of NASH. Long term administration of PPARgamma activator pioglitazone ameliorated the activity of NASH. In this review, we summarize the evidences concerning NASH and PPAR in this time.

Publication types

  • Review

MeSH terms

  • Acyl-CoA Oxidase / genetics
  • Animals
  • Cytokines / physiology
  • Fatty Liver / drug therapy
  • Fatty Liver / etiology*
  • Gene Deletion
  • Humans
  • Inflammation Mediators / physiology
  • Insulin Resistance
  • Liver Cirrhosis / etiology
  • Mice
  • Mice, Knockout
  • Oxidative Stress
  • Peroxisome Proliferator-Activated Receptors / genetics
  • Peroxisome Proliferator-Activated Receptors / physiology*
  • Peroxisomes / physiology
  • Pioglitazone
  • Protein Isoforms
  • Thiazolidinediones / administration & dosage

Substances

  • Cytokines
  • Inflammation Mediators
  • Peroxisome Proliferator-Activated Receptors
  • Protein Isoforms
  • Thiazolidinediones
  • Acyl-CoA Oxidase
  • Pioglitazone