Table 2.
Models | Advantages | Disadvantages |
---|---|---|
Ad libitum model | Easy to perform. Minimal elevation of ALT and mild steatosis. Short-or long-term feeding with no mortality rate. |
Insufficient for fibrosis or cirrhosis. Desired BAC levels cannot be achieved. |
Lieber–DeCarli model | Easy to perform. Increase in hepatic triglycerides. CYP2E1 induction, marked elevation of AST and ALT. Reactive oxygen species production. mild steatosis. infiltration of inflammatory cells can be observed. |
It is not physiological. No liver fibrosis. |
The Tsukamoto–French intragastric infusion model | Marked elevation of AST and ALT and steatosis. |
Difficult to perform. Requirement for intensive medical care. Expensive materials required. Mild liver fibrosis. Long-term feeding with a high mortality rate. |
The NIAAA Model | Cost and time efficient. High blood alcohol levels. Liver injury. Inflammation. Fatty liver. |
Animals to which the model is applied experience high weight loss and the mortality of the model is also high. |
Secondary intervention methods | Simple and cheap. Moderate to significant elevation of serum ALT, AST, and liver. inflammation dependent on second hit. Liver fibrosis. Liver cancer. |
Time consuming. Toxic components. |
ALT, alanine aminotransferase; AST, aspartate aminotransferase; BAC, blood alcohol concentration.