Alcohol deranges hepatic lipid metabolism via altered transcriptional regulation.

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Abstract

Alcohol has classically been thought to cause fatty liver by way of altered redox potential in the liver, which inhibits fatty acid oxidation. Additional effects appear to play a role both in impairing fat oxidation and stimulating lipogenesis. Alcohol reduces the DNA binding and transcription-activating properties of peroxisome proliferator-activated receptor alpha (PPARalpha), both in cultured cells and in mice fed alcohol. Treatment of alcohol-fed mice with a PPARalpha agonist reverses fatty liver despite continued alcohol consumption. Alcohol also activates sterol response element- binding protein 1 (SREBP-1), inducing a battery of lipogenic enzymes. This effect may be due in part to inhibition of AMP-dependent protein kinase. This understanding of alcohol effects provides new therapeutic targets to reverse alcoholic fatty liver.

Original languageEnglish (US)
Pages (from-to)273-287
Number of pages15
JournalTransactions of the American Clinical and Climatological Association
Volume115
StatePublished - 2004

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ASJC Scopus subject areas

  • Medicine(all)

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