Contribution of de novo fatty acid synthesis to hepatic steatosis and insulin resistance: lessons from genetically engineered mice

J Clin Invest. 2008 Mar;118(3):829-38. doi: 10.1172/JCI34275.

Abstract

Nonalcoholic fatty liver disease (NAFLD) is associated with obesity, insulin resistance, and type 2 diabetes. NAFLD represents a large spectrum of diseases ranging from (i) fatty liver (hepatic steatosis); (ii) steatosis with inflammation and necrosis; and (iii) cirrhosis. Although the molecular mechanism leading to the development of hepatic steatosis in the pathogenesis of NAFLD is complex, recent animal models have shown that modulating important enzymes in fatty acid synthesis in liver may be key for the treatment of NAFLD. This review discusses recent advances in the field.

Publication types

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

MeSH terms

  • Acetyl-CoA Carboxylase / antagonists & inhibitors
  • Acetyltransferases / antagonists & inhibitors
  • Animals
  • Fatty Acid Synthases / physiology
  • Fatty Acids / biosynthesis*
  • Fatty Liver / etiology*
  • Fatty Liver / metabolism
  • Fatty Liver / prevention & control
  • Humans
  • Insulin Resistance*
  • Lipoproteins, VLDL / biosynthesis
  • Liver / metabolism*
  • Mice
  • Mice, Transgenic
  • Nuclear Proteins / physiology
  • Stearoyl-CoA Desaturase / deficiency
  • Transcription Factors / physiology
  • Triglycerides / biosynthesis

Substances

  • Fatty Acids
  • Lipoproteins, VLDL
  • Mlxipl protein, mouse
  • Nuclear Proteins
  • Transcription Factors
  • Triglycerides
  • SCD1 protein, human
  • Stearoyl-CoA Desaturase
  • Acetyltransferases
  • aminoglycoside N1-acetyltransferase
  • Fatty Acid Synthases
  • ACACB protein, human
  • Acetyl-CoA Carboxylase