Recent advances in alcoholic liver disease - II. Minireview: Molecular mechanisms of alcoholic fatty liver

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179 Scopus citations


Alcohol has long been thought to cause fatty liver by way of altered NADH/NAD+ redox potential in the liver, which, in turn, inhibits fatty acid oxidation and the activity of tricarboxylic acid cycle reactions. More recent studies indicate that additional effects of ethanol both impair fat oxidation and stimulate lipogenesis. Ethanol interferes with DNA binding and transcription-activating properties of peroxisome proliferator-activated receptor-α (PPARα), as demonstrated with cultured cells and in ethanol-fed mice. Treatment of ethanol-fed mice with a PPARα agonist can reverse fatty liver even in the face of continued ethanol consumption. Ethanol also activated sterol regulatory element binding protein 1, inducing a battery of lipogenic enzymes. These effects may be due in part to inhibition of AMP-dependent protein kinase, reduction in plasma adiponectin, or increased levels of TNF-α in the liver. The understanding of these ethanol effects provides new therapeutic targets to reverse alcoholic fatty liver.

Original languageEnglish (US)
Pages (from-to)G1-G6
JournalAmerican Journal of Physiology - Gastrointestinal and Liver Physiology
Issue number1 50-1
StatePublished - Jul 1 2004



  • Ethanol
  • Lipid
  • Transcription factor
  • Triglyceride

ASJC Scopus subject areas

  • Gastroenterology
  • Physiology

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