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. Three condition experiment - control (maltose), 5g/kg EtOH gavage, 7g/kg EtOH gavage