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- W3176266772 abstract "Liver injury caused by heavy alcohol consumption progresses from steatosis to steatohepatitis in some individuals. Binge ethanol intake is important factor in the progression to steatohepatitis in chronic alcoholics. Recent studies have implicated activation of extracellular regulated kinases (ERK1/2) to the actions of ethanol in cultured hepatocytes. In the present study, role of of ERK1/2 was examined in a clinically relevant animal model of progressive liver injury. This involved chronic ethanol administration for 4 weeks followed by a binge dose of ethanol (chronic-binge) that culminated in an amplified liver injury. Eight week old Sprague Dawley rats were fed ethanol in liquid diet for 4 weeks followed by single binge dose of ethanol (5 gm/kg body weight) through intragastric administration for 4 hrs. Control rats were pair-fed isocaloric diet. In the control for the binge ethanol was replaced by water. Chronic ethanol treatment (4 weeks) resulted in mild steatosis and necrosis whereas chronic- binge group exhibited marked steatosis and significant increase (2 fold) in necrosis. Chronic - binge group also showed significant increase (2 to 3 fold) in the phospho-ERK1/2 in liver with negligible effect on ERK1/2 protein level. Activation of ERK1/2 was not significant in the liver of ethanol alone treated group compared to control group. Taken together, these results suggest that activation of ERK1/2 by binge ethanol may augment steatosis and necrosis in liver. Supported by NIH grant AA 11962." @default.
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- W3176266772 date "2009-04-01" @default.
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- W3176266772 title "Activation of ERK1/2 MAP kinase in rat liver in vivo after binge and chronic‐binge ethanol intake may augment liver injury" @default.
- W3176266772 doi "https://doi.org/10.1096/fasebj.23.1_supplement.760.3" @default.
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