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食用台湾自助餐厅饮食会导致肥胖大鼠代谢紊乱和粪便菌群改变。

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

机构信息

School of Nutrition and Health Sciences, Taipei Medical University, Taipei, Taiwan.

Graduate Institute of Health Industry Technology, Research Center for Food and Cosmetic Safety, Research Center for Chinese Herbal Medicine, College of Human Ecology, Chang Gung University of Science and Technology, Taiwan.

出版信息

Nutrition. 2024 Jan;117:112230. doi: 10.1016/j.nut.2023.112230. Epub 2023 Sep 22.

Abstract

OBJECTIVES

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.

METHODS

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).

RESULTS

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.

CONCLUSIONS

The present study confirmed that the Taiwanese cafeteria diet-induced rat model provided a potential platform for investigating obesity-related diseases.

摘要

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