Table 1.

Summary of fatty liver disease findings from studies performed in mice that exhibit a genetic defect in genes critically involved the HDL life cycle.

Genotype	Gender	Age at start	Type of diet	Diet composition	Time on diet	HDL-C	NAFLD extent	Liver lipid phenotype	Reference
ABCA1 KO mice	Unknown	2 weeks-10 months	Western	20.85% raw fat, 0.15% cholesterol, 19.5% casein	10 days	↓	↓	Cholesteryl ester ↓	[52]
apoA1 KO mice	Male	10–12 weeks	Western	17.3% protein, 48.5% carbohydrate, 21.2% fat, 0.2% cholesterol	18 weeks	↓	= /↑	Triglyceride = Cholesterol ↑	[50]
					24 weeks	↓	↑	Triglyceride ↑ Cholesterol ↓	[49]
apoA1 overexpressing C57BL/6 mice	Male	4–6 weeks	Methionine Choline-deficient	Details unknown	1 week	↑	↓	Triglyceride ↓ Cholesterol ↓	[53]
PLTP KO mice	Both	12 weeks	Low fat	18% protein, 5% fat	12 weeks	↓	females: ↓↑ males: ↓	Cholesterol = /↑ Triglyceride ↓	[51]
SR-BI KO mice	Male	8–11 weeks	High fat	45% fat, 20% protein	12 weeks	↑	↓	Triglyceride ↓ Cholesterol=	[54]
	Male	10–12 weeks	Western	17.3% protein, 48.5% carbohydrate, 21.2% fat, 0.2% cholesterol	24 weeks	↑	↓	Triglyceride ↓ Cholesterol ↑	[55]
CETP Tg mice + anacetrapib treatment	Male	Unknown	High fat	60% fat, 20% protein	3 months	↑	↑	Triglyceride ↑ Cholesterol ↓	[61]

Arrows indicate the effect on the specific parameter as compared to normolipidemic wild-type controls or untreated CETP Tg mice, respectively.