Ethanol and its nonoxidative metabolites promote acute liver injury by inducing ER stress, adipocyte death and lipolysis. Ethanol and its nonoxidative metabolites promote acute liver injury by inducing ER stress, adipocyte death and lipolysis

We gave mice either a 5g/kg ethanol (EtOH) gavage, a 7g/kg EtOH gavage, or an isocaloric maltose gavage (equivalent to 5g/kg EtOH) in the morning and sacrificed mice 9h later. Microarray analyses were performed on liver tissue from these mice to determine genes and pathways contributing to acute ethanol-induced liver injury. Lipid metabolism-associated genes were found to be dysregulated in both the 5g/kg and 7g/kg groups, with the majority of changes occuring in the 7g/kg group. Genes related to fatty acid metabolism were most changed in the 7g/kg group compared to control and 5g/kg groups. Overall design: Three condition experiment - control (maltose), 5g/kg EtOH gavage, 7g/kg EtOH gavage