TABLE 2.

Study design factors to consider in diet-induced nonalcoholic fatty liver disease rodent models¹

	High-fat diets	High-fructose diets	High-fat, -fructose, and -cholesterol diets	Choline-deficient high-fat diets	Methionine- and choline-deficient diets
Dietary modifications commonly used	30–60 kcal% fat, higher SFAs increase ER stress, higher ω-6 PUFAs increase increase oxidative stress, both increase NASH More sucrose or fructose leads to NASH and mild fibrosis	Usually 60–70 kcal% fructose drives steatosis, NASH The addition of sucrose (50%fructose) also effective effective for steatosis, NASH	40 kcal% fat (trans fat or SFAs), 20–40 kcal% fructose, and 1–2% cholesterol Fat type and cholesterol increase ER and oxidative stress/fibrosis Fructose drives steatosis and inflammation	Fat amount (30–60 kcal% fat) Lard commonly used; typically can drive steatosis, but prolonged feeding (6 mo) can cause fibrosis	Rapid onset of steatosis (1 wk), NASH/fibrosis in 6–8 wk Addition of fat (≤60 kcal% fat) Fat type typically lard, butter (SFAs), or corn oil (PUFAs), addition of sucrose and/or cholesterol drives further NASH/fibrosis
Other metabolic effects	Increases body weight IR/glucose intolerance	Increases body weight IR/glucose intolerance Increased plasma TGs (typically ratsand hamsters)	Increases body weight IR/glucose intolerance Increases plasma lipids	Increases body weight Less IR than choline-sufficient diet	Reduces body weight, but 0.1% methionine maintains weight No IR, reduced plasma lipids
Matched control diet	Low-fat diet with matched amount of sucrose or mostly corn starch	Low-fat diet with 60–70 kcal% as either glucose or corn starch	Low-fat diet with 60–70 kcal% as either glucose or corn starch	Low-fat diet with choline	Methionine- and choline-sufficient diet

¹ER, endoplasmic reticulum; IR, insulin resistance; NASH, nonalcoholic steatohepatitis; TG, triglyceride.