[Obesity and liver disease]

Gastroenterol Hepatol. 2010 Oct;33(8):591-604. doi: 10.1016/j.gastrohep.2009.12.009. Epub 2010 Mar 4.
[Article in Spanish]

Abstract

Obesity is associated with a higher risk of developing non-alcoholic fatty liver disease (NAFLD) and contributes to the progression of liver diseases of distinct etiologies such as chronic hepatitis C virus (HCV) infection. The discovery that adipose tissue is submitted to a state of chronic inflammation able to secrete adipokines has allowed a connection to be established between the metabolic alterations that lead to triglyceride accumulation and liver inflammation, reinforcing the role of hepatocellular lipotoxicity in the pathogenesis of NAFLD. In addition, although HCV genotype 3 induces steatosis, it is currently believed that obesity and its associated alterations, such as insulin resistance, are involved in progression of HCV-mediated liver disease, as well as that of other chronic liver diseases of diverse etiologies.

Publication types

  • Review

MeSH terms

  • Adenylate Kinase / physiology
  • Adipokines / metabolism
  • Adipose Tissue / metabolism
  • Animals
  • Disease Progression
  • Fatty Acids / metabolism
  • Fatty Liver / etiology
  • Fatty Liver / physiopathology
  • Hepatitis C, Chronic / complications
  • Humans
  • Inflammation
  • Insulin Resistance
  • Lipid Metabolism
  • Lipid Peroxidation
  • Liver Diseases / etiology*
  • Liver Diseases / physiopathology
  • Liver X Receptors
  • Mice
  • Mice, Knockout
  • Models, Biological
  • Obesity / classification
  • Obesity / complications*
  • Obesity / epidemiology
  • Obesity / physiopathology
  • Orphan Nuclear Receptors / physiology
  • PPAR alpha / physiology
  • Triglycerides / metabolism

Substances

  • Adipokines
  • Fatty Acids
  • Liver X Receptors
  • Orphan Nuclear Receptors
  • PPAR alpha
  • Triglycerides
  • Adenylate Kinase