Consumption of a Taiwanese cafeteria diet induces metabolic disorders and fecal flora changes in obese rats

•The Taiwanese cafeteria diet induced rapid weight gain and fat accumulation in rats after 12 wk.•Compared with the traditional high-fat diet, cafeteria diet consumption led to higher hepatic inflammatory cytokines, which then contributed to insulin resistance.•The cafeteria diet disrupted microbiome composition, which may be associated with obesity.•The Taiwanese cafeteria diet has greater potential to be a model of obesity-related disease than the traditional high-fat diet. Among diet-induced obesity animal models, the cafeteria diet, which contains human junk food and processed foods, is a popular experimental animal diets in Western countries. Consumption of a cafeteria diet can lead to the development of obesity and non-alcoholic liver disease in as soon as 2 mo, which more accurately reflects human eating patterns. The aim of this study was to establish a Taiwanese cafeteria diet and compare it with a traditional lard-based, 60% high-fat diet in a 12-wk animal model. Six-wk-old male Wistar rats were assigned to the following three groups: control diet (C; LabDiet 5001); high-fat diet (HFD; 60% HFD); and the Taiwanese cafeteria diet (CAF). At the end of the study, weight gain and steatosis were observed in the HF and CAF groups. Compared with the HFD group, rats in the CAF group showed significantly higher plasma triacylglycerol concentrations and insulin resistance, which may have been correlated with increased inflammatory responses. Significantly lower hepatic sterol regulatory element-binding protein-1c and insulin receptor substrate-1 protein expressions were observed in the CAF group compared with the HFD group. Additionally, disruption of the microbiotic composition followed by increased obesity-related bacteria was observed in the CAF group. The present study confirmed that the Taiwanese cafeteria diet-induced rat model provided a potential platform for investigating obesity-related diseases.