Even though the specific etiology of NAFLD remains unclear, dietary fat and cholesterol have been linked to the development of hepatic steatosis and NASH in both humans and animal models [12–14] and more recently, the marked increase in consumption of the simple carbohydrate fructose, has been pointed out as another possible contributory factor [15, 16]. The realization that diet is an important contributor to the pathogenesis of NAFLD has resulted in a considerable variety of diet-induced animal models, where the majority (apart from those based on nutritional deficiencies) is based on a high-fat diet with varying levels of simple carbohydrate and cholesterol [17, 18]. However, the individual roles of fat, carbohydrates and cholesterol in the development of NAFLD are still not entirely clear. Thus, improved insight from animal studies on the individual contribution of fat, simple carbohydrates and cholesterol to the metabolic and inflammatory characteristics of NAFLD is an important prerequisite in understanding the disease complexity in patients. Furthermore, establishment of animal models of NAFLD/NASH that more adequately mimic human pathology will be valuable when testing novel therapeutics for NAFLD/NASH.