Background and aims: Drug-induced fatty liver disease (DIFLD) has become a common cause of non-alcoholic fatty liver disease (NAFLD) due to the aging of the population and the prevalence of polypharmacy in the elderly. It is possible for NAFLD and DIFLD to coexist which makes it even more crucial to be able to differentiate them. Our aim was to investigate hepatocyte steatosis NAFLD and DIFLD cell culture models and ascertain the effects of liraglutide in those models. Materials and Methods: To create models of hepatocyte steatosis NAFLD and DIFLD, Huh7 cells were treated with oleic acid, amiodarone, or tamoxifen. Liraglutide was administered to the cells, and MTT was used to measure cell viability, while Erythrosin B color exclusion test was used to confirm results for cell survival. Oil-Red-O staining and a triglyceride assay were used to measure lipid accumulation, GSH assay kit was used for the measurement of GSH concentrations in all three models, and RT-PCR was used to measure intracellular signals involved in hepatosteatosis. Results: The concentrations of oleic acid, amiodarone, and tamoxifen that achieved 80% cell viability comparing to the negative control were used in subsequent experiments to establish the NAFLD and DIFLD models. Those were 0.5 mM oleic acid, 20 µM amiodarone, and 2 µM tamoxifen, respectively. Liraglutide improved cell viability in all models (p < 0,01). All models showed increased lipid accumulation, with DIFLD showing a microsteatotic pattern and NAFLD showing a macrosteatotic pattern, the latter of which corresponds to greater triglyceride accumulation. These steatotic changes were lessened by liraglutide (p < 0,001). GSH levels were reduced in all three models of steatosis. Amiodarone and tamoxifen reduced it to 80% compared to DMEM negative control (p < 0,01, p < 0,05), while effect of OA was smaller. There was no significant difference in GSH concentrations with liraglutide co-treatment. In the hepatocyte steatosis NAFLD and DIFLD models, liraglutide decreased the expression of the lipogenic ACSL1, PPARG, and SREBF1 pathways (p < 0,01). Conclusion: In hepatocyte steatosis NAFLD and DIFLD models established with Huh7 cell culture, liraglutide reduced hepatocyte steatosis through downregulation of lipogenic ACSL1, PPARG, and SREBF1 pathways.