As mentioned above, ethanol induced steatosis in WT and KI mice but to a much lesser extent in KO mice. Further evaluation showed elevated oil red staining in WT and KI mice to a greater extent than in KO mice (Fig. 3E). The oil red staining, similar to the histopathology suggested a more elevated steatosis in the WT mice as compared to the KI mice. Hepatic triglycerides were elevated by ethanol about two-fold in the KO mice, about seven-fold in the KI mice and about three-fold in the WT mice (Fig. 2D). Triglyceride levels were higher in both the dextrose-fed and ethanol-fed WT mice than the corresponding KO and KI mice, likely accounting for the “only” three fold increase by ethanol in WT mice compared to the 7-fold increase in KI mice. The steatosis score confirmed that ethanol produced fatty liver in the WT and KI mice, but not the KO mice (Fig. 2F). Interestingly, while the steatosis score was highest in the ethanol-fed WT mice, the necroinflammatory score was highest in the ethanol-fed KI mice. Both scores were lowest in the ethanol KO mice.
