Table 2.
Animal models of alcoholic liver injury
| Model | Comments | Steatosis | Inflammation and necrosis | Fibrosis and cirrhosis |
|---|---|---|---|---|
| Ad libitum | ||||
| Drinking water | Not relevant due to the lack of significant pathology | –/– | –/– | –/– |
| Liquid diet | Reliable method to model early fatty changes caused by alcohol exposure. Easy to employ and well characterized. Pathology does not progress much past steatosis. | ++ | + | –/+ |
| Enteral feeding | ||||
| Liquid diet | Causes enhanced liver pathology due to higher levels of ethanol. Relevance of high doses of ethanol to humans a concern. | +++ | ++ | –/+ |
| Alternative models | ||||
| Choline deficiency | Dietary model that mimics all stages of human ALD, including hepatocellular carcinoma. Relevance of lipotrope deficiency to humans is questionable. | +++ | +++ | +++ |
| Other hepatotoxins (e.g. CCl4, TAA, DMNS) | Can cause severe fibrosis or cirrhosis relatively rapidly. Severity of liver damage is usually higher than that of ALD. | –/+ | +++ | +++ |
General animal models utilized in the study of alcoholic liver disease.