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Chronic Ethanol Feeding Alters Hepatocyte Memory Which is not Altered by Acute Feeding
Author(s) -
BardagGorce F.,
Oliva Joan,
Dedes Jennifer,
Li Jun,
French Barbara A.,
French Samuel W.
Publication year - 2009
Publication title -
alcoholism: clinical and experimental research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.267
H-Index - 153
eISSN - 1530-0277
pISSN - 0145-6008
DOI - 10.1111/j.1530-0277.2008.00885.x
Subject(s) - ethanol , gene expression , epigenetics , microarray , dna methylation , endocrinology , ethanol metabolism , medicine , microarray analysis techniques , methylation , alcohol dehydrogenase , liquid diet , biology , gene , biochemistry
Background:  Gene expression changes in the liver after acute binge drinking may differ from the changes seen in chronic ethanol feeding in the rat. The changes in gene expression after chronic ethanol feeding may sensitize the liver to alcohol‐induced liver damage, which is not seen after acute binge drinking. Methods:  To test this hypothesis, gene microarray analysis was performed on the livers of rats ( n  = 3) fed an acute binge dose of ethanol (6 g/kg body wt) and killed at 3 and 12 hours after ethanol by gavage. The gene microarrays were compared with those made on the liver of rats from a previous study, in which the rats were fed ethanol by intragastric tube for 1 month (36% of calories derived from ethanol). Results:  Microarray analysis data varied between the acute and chronic models in several important respects. Growth factors increased mainly in the chronic alcohol fed rat. Changes in enzymes involved in oxidative stress were noted only with chronic ethanol feeding. Gene expression of fat metabolism was increased only with chronic ethanol feeding. Most importantly, epigenetic related enzymes and acetylation and methylation of histones changed only after chronic ethanol feeding. Conclusions:  The results support the concept that chronic ethanol ingestion induces altered gene expression as a result of changes in epigenetic mechanisms, where acetylation and methylation of histones were altered.

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