Animal models of liver disease are fundamentally important to strengthen our knowledge and understanding of human liver diseases. Murine models of alcohol consumption are utilized to investigate alcoholic liver injury to develop new therapeutic targets. The well accepted and commonly used murine models of chronic alcohol consumption are Meadows-Cook (MC) and Lieber-DeCarli (LD). LD model is based on an isocaloric high-fat liquid diet, but mice under the MC model fed on a regular chow diet with alcohol added to the drinking water. Alcoholic liver disease in real world is frequently diagnosed in patients with obesity and high fat intake, mirroring LD diet. The overlap of the specific effect of ethanol and obesity is difficult to differentiate by clinician and pathologist. In this commentary, we will further discuss our research findings comparing MC and LD as a tool to dissect early alcohol versus increased fat intake detrimental effects on the liver. The critical analysis of these two models could provide evidence to differentiate the specific impact of alcohol on the liver from the combined influence of alcohol and diet. Ultimately, these investigations could uncover potential biomarkers and therapeutic targets for personalized type of alcoholic liver injury.
Alcoholic liver disease (ALD); Mouse; Meadows-Cook (MC); Lieber-DeCarli (LD); Patatin-like phospholipase domain containing 3 (Pnpla3); Lipocalin-2 (Lcn2); ELOVL Fatty Acid Elongase 6 (Elovl6); Sulfotransferase family 2A, member 3 (Sult2a3)