Table 1.

Commonly used animal models for ALD

Models	Characteristics	·Mechanisms
Acute binge ethanol feeding model	·Mild elevation of serum ALT, AST	·Damages hepatocyte mitochondrial functions and produces oxidative stress
	·Low levels of liver inflammation with a decrease in hepatic macrophages
	·Easy to perform
Chronic ethanol feeding (Lieber-DeCarli model)	·Mild elevation of serum ALT, AST	·Increases gut permeability and activates LPS-TLR4-Kupffer cells ·Damages hepatocyte mitochondrial functions and produces oxidative stress
	·Low levels of liver inflammation with an increase in macrophages but not neutrophils
	·Easy to perform
Intragastric chronic ethanol feeding (Tsukamoto-French model)	·Moderate elevation of serum ALT, AST	·Similar mechanisms as chronic ethanol feeding
	·Moderate liver inflammation with an increase in macrophages but low levels of neutrophils
	·Difficult to perform
“Second hit” or “Multiple hits” model	·Moderate to significant elevation of serum ALT, AST, and liver inflammation dependent on second hit	·Chronic ethanol feeding increases susceptibility of livers to second or multiple hit(s)-induced liver injury and inflammation
	·Easy to perform
Chronic+binge feeding model (Gao-binge model)	·Moderate elevation of serum ALT, AST	·Increases hepatic neutrophil infiltration and subsequently induces liver injury ·Damages hepatocyte mitochondrial functions and produces oxidative stress
	·Moderate liver inflammation with an increase in neutrophils
	·Easy to perform
Tsukamoto-hybrid model with high-cholesterol and high-fat diet plus chronic ethanol and binge ethanol feeding	·Significant elevation of serum ALT, AST	·Increases hepatic neutrophil and macrophage infiltration and subsequently induces liver injury ·Damages hepatocyte mitochondrial functions and produces oxidative stress
	·Significant liver inflammation with an increase in neutrophils
	·Mild liver fibrosis
	·Difficult to perform

ALD, alcoholic liver disease; ALT, alanine aminotransferase; AST, aspartate aminotransferase.