Table 2.

Animal Models of nonalcoholic fatty liver disease

Model	Mechanisms	Salient Features	References
Dietary Deficiency
Methionine choline deficient	Impaired VLDL secretion from liver	Features of steatohepatitis in 10 weeks But in presence of weight loss and improved insulin sensitivity	(Caballero et al., 2010; Oz, Chen, & Neuman, 2008)
Conjugated Linoleic Acid (CLA)	Diet with transfat conjugated with linoleic acid	Features of steatohepatitis with mild peri-sinusoidal fibrosis with insulin resistance and near universal HCC development But in presence of weight loss and improved insulin sensitivity	(Fujita et al., 2010)
Choline-def L-AA (CDAA)	Diet deficient in choline; containining only L-amino acids	Develops fibrosing NASH, cirrhosis and HCC. But in presence of weight loss, improved insulin sensitivity and increasing adiponectin levels	(de Lima et al., 2008)
Dietary Excess
High Fat Diet	> 60% fat calories	Steatosis with minimal and variable inflammation and fibrosis associated with obesity, insulin resistance and dyslipidemia.	(Tetri, Basaranoglu, Brunt, Yerian, & Neuschwander-Tetri, 2008)
Western Diet	45% saturated and trans fats High cholesterol	Steatohepatitis w/ballooning and variable fibrosis But takes up to 20 weeks	(Kohli et al., 2010)
Atherogenic diet	1.25% cholesterol and 0.5% cholate	Steatohepatitis with ballooning and fibrosis But occurs in setting of weight loss and improved insulin sensitivity and takes up to 24 weeks	(Charlton et al., 2011)
Genetic Models
ob/ob	Mutation in leptin	Steatosis, Steatohepatitis develops after 2nd hit in obese, hyperphagic, inactive animals that show insulin resistance and dyslipidemia But resistant to fibrosis	(Ingalls, Dickie, & Snell, 1950; Zhang et al., 1994)
db/db	Mutation in leptin receptor	Steatohepatitis after 2nd hit in obese animals with insulin resistance	(Chen et al., 1996; Hummel, Dickie, & Coleman, 1966)
ApoE KO	Absence of ApoE protein, a ligand of the LD receptor	Steatohepatitis after 2nd hit in animals with increased LDL, total cholesterol and triglycerides and atherosclerosis Model of dyslipidemia	(Schierwagen et al., 2015)
aP2-nSREBP-1c transgenic	Over-exp of SREBP-1c in adipose tissue	Steatohepatitis with mild fibrosis in animals with increased Glu; decreased adiponectin Model of lipodystrophy	(Shimano et al., 1996)
MAT1A KO	Absence of methionine adenosyltranfer ase (impaired anti-oxidant defense)	Steatohepatitis without fibrosis with high susceptibility to tumors But no evidence of metabolic syndrome,	(Lu et al., 2001)