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Genetic difference between A/J and C57BL/6J mice response to chronic alcohol consumption.
Author(s) -
Croniger Colleen Marie,
DeSantis David,
Pisano Sorana,
Millward Carrie,
Hsieh ChangWen,
Nagy Laura
Publication year - 2009
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.23.1_supplement.981.4
Subject(s) - steatosis , liver injury , genetic predisposition , endocrinology , medicine , pathophysiology , alcoholic liver disease , gene , tumor necrosis factor alpha , biology , fatty liver , inbred strain , gene expression , genetics , disease , cirrhosis
Genetics contributes to susceptibility and development of disease. In the present study, the response to chronic alcohol was studied in two inbred strains, C57BL/6J and A/J. We report that the C57BL/6J mice developed steatosis with an increase expression of CCAAT/enhancer‐binding protein β (C/EBPβ) gene. The A/J mice were resistant to the development of steatosis due to a decreased C/EBPβ gene expression. However the A/J mice develop liver injury with increased levels of alanine aminotransferase (ALT), aspartate aminotransferase (AST) and tumor necrosis factor α (TNFα) that is decoupled from hepatic lipid accumulation, suggesting that other mechanisms contribute to alcohol induced liver injury. These data demonstrate that genetics contribute to the pathophysiology of alcohol‐induced liver injury.