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Updated: Mar 22, 2026
Palatable Western-style Cafeteria Diet as a Reliable Method for Modeling Diet-induced Obesity in Rodents
Published on: November 1, 2019
An ultra-processed food-based cafeteria diet induces obesity, metabolic dysfunction, and tissue-specific gene
Guilherme Coutinho Kullmann Duarte1,2, Daisy Crispim1,3, Shiva Cerutti Wittée3
1Post-Graduate Program in Medical Sciences: Endocrinology, Faculdade de Medicina, Universidade Federal do Rio Grande do Sul, Porto Alegre, Brazil.
Background:
The cafeteria diet (CAFD) model has been used to mimic the Western-style "junk food" eating pattern, inducing obesity in rodents. As the dietary composition varies across studies, we developed a CAFD model based on commonly consumed Brazilian ultra-processed foods to evaluate its effect on weight gain, metabolic parameters, and gene expression in C57BL/6 mice.
Methods:
Forty male C57BL/6 mice were assigned to either a standard diet (SD) group or a CAFD group for 16 weeks. Biometric data, glycemic control, insulin resistance (IR), hepatic steatosis, and serum leptin and adiponectin levels were assessed. Expressions of 27 genes involved in adipocytokine signaling, inflammation, apoptosis, lipid, and glucose metabolism were analyzed using quantitative real-time polymerase chain reaction in visceral (VAT) and subcutaneous (SAT) adipose tissues, liver, and skeletal muscle.
Results:
CAFD-fed mice exhibited significantly greater weight gain, hyperglycemia, elevated IR, and hepatic steatosis compared to SD controls. Circulating leptin and adiponectin levels increased in the CAFD group. Gene expression analysis revealed significant dysregulation in VAT (19 genes), SAT (6 genes), liver (11 genes), and muscle (4 genes) of the CAFD group, affecting pathways related to adipocytokine signaling, oxidative stress, inflammation, apoptosis, and lipid and glucose metabolism. Additionally, an increased Itgax-to-Llgl1 ratio in VAT of the CAFD mice indicated a phenotypic shift in macrophages from M2 to pro-inflammatory M1.
Conclusion:
This CAFD model efficiently induces obesity, metabolic dysfunction, and tissue-specific alterations in gene expression in C57BL/6 mice, supporting its use as a relevant model for studying the molecular and inflammatory mechanisms underlying diet-induced obesity.
