Alcohol deranges hepatic lipid metabolism via altered transcriptional regulation.

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11 Citations (Scopus)

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

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Lipid Metabolism
Alcohols
Liver
PPAR alpha
Fatty Liver
Alcoholic Fatty Liver
Lipogenesis
Response Elements
Sterols
Adenosine Monophosphate
Alcohol Drinking
Protein Kinases
Oxidation-Reduction
Cultured Cells
Carrier Proteins
Fatty Acids
Fats
DNA
Enzymes

ASJC Scopus subject areas

  • Medicine(all)

Cite this

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