Experimental research has successfully established an adult offspring animal model of nonalcoholic fatty liver disease (NAFLD), but the female offspring model of NAFLD in young age has not been well characterized yet. The aim of this study was to present a direct comparison of the maternal versus postweaning female juvenile NAFLD and nonalcoholic steatohepatitis (NASH) animal models. Four different female mouse models were established and compared using different high-fat diet feeding (HF) strategies in maternal mice and their offspring. The models were non-HF maternal mice and HF offspring with high-high fat (C/HHF), non-HF maternal mice and HF offspring with low-high fat (C/LHF), HF maternal mice and offspring both with high-high fat (HHF/HHF), and HF maternal mice and offspring both with low-high fat (LHF/LHF). A female control group (C/C) was also established. The offspring mice were raised to the age of 8 weeks and then euthanized. Blood glucose levels, lipid profiles, liver function, and triglycerides/total cholesterol contents were examined. Hepatic morphology and superoxide anion levels were evaluated. The nicotinamide-adenine dinucleotide phosphate activity and related regulatory subunits protein expression in the liver tissue were also determined. Our data demonstrated that offspring fat intake contributed to the successful establishment of NAFLD and maternal-offspring fat intake contributed to the successful establishment of NASH in juvenile female mice. Offspring high-fat exposure might be associated with the development of NAFLD and maternal high-fat exposure might be associated with the development of NASH in juvenile female offspring. Higher calories from a fat diet program (both in maternal and offspring) are more prone to inducing liver injury in offspring. In addition, the combination of the aforementioned two factors could aggravate this process. Moreover, oxidative stress was prominent in the juvenile female mouse model of NAFLD/NASH, and the mechanism might be related to the activation of liver NADPH oxidase.