Nonalcoholic fatty liver disease: molecular mechanisms for the hepatic steatosis

Clin Mol Hepatol. 2013 Sep;19(3):210-5. doi: 10.3350/cmh.2013.19.3.210. Epub 2013 Sep 30.

Abstract

Liver plays a central role in the biogenesis of major metabolites including glucose, fatty acids, and cholesterol. Increased incidence of obesity in the modern society promotes insulin resistance in the peripheral tissues in humans, and could cause severe metabolic disorders by inducing accumulation of lipid in the liver, resulting in the progression of non-alcoholic fatty liver disease (NAFLD). NAFLD, which is characterized by increased fat depots in the liver, could precede more severe diseases such as non-alcoholic steatohepatitis (NASH), cirrhosis, and in some cases hepatocellular carcinoma. Accumulation of lipid in the liver can be traced by increased uptake of free fatty acids into the liver, impaired fatty acid beta oxidation, or the increased incidence of de novo lipogenesis. In this review, I would like to focus on the roles of individual pathways that contribute to the hepatic steatosis as a precursor for the NAFLD.

Keywords: De novo lipogenesis; Fatty acid beta oxidation; Free fatty acids; TG secretion.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Acetyl Coenzyme A / metabolism
  • Fatty Acids / metabolism
  • Fatty Liver / metabolism*
  • Fatty Liver / pathology
  • Humans
  • Lipogenesis
  • Mitochondria / metabolism
  • Non-alcoholic Fatty Liver Disease
  • Triglycerides / metabolism

Substances

  • Fatty Acids
  • Triglycerides
  • Acetyl Coenzyme A