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Updated: Apr 14, 2026

Palatable Western-style Cafeteria Diet as a Reliable Method for Modeling Diet-induced Obesity in Rodents
Published on: November 1, 2019
Maternal Programming with a Cafeteria Diet Leads to Glucose Intolerance, Increased Insulinemia, Inflammation, and
Dayane Correia Gomes1, Jesús Alejandro Zamora-Briseño2, Alberto Camacho Morales3
1Postgraduate Program in Biomedical Sciences, Biomedical Research Center, Universidad Veracruzana, Veracruz 91190, México.
Abstract:
The intake of diets high in fat and sugar but low in protein, fiber, and vitamins during pregnancy can contribute to metabolic imbalance, immunological disorders, and intestinal barrier disruption in the offspring. This study investigated the effects of a cafeteria (CAF) diet, high in fat and sugar, consumed throughout pregnancy and lactation, on metabolism, inflammation-related markers, and intestinal microbiota in rat offspring. Maternal programming was conducted for more than 9 weeks in 16 female Wistar rats aged 8-10 weeks. They were divided into two diet groups: control and CAF, each with n=8. On the 21st day after birth, the offspring were weaned, and fecal samples were collected. We conducted a series of glucose and insulin tolerance tests and analyzed serum metabolic markers [triglycerides (TGs), total cholesterol (TC), aspartate aminotransferase (AST), alanine aminotransferase (ALT), alkaline phosphatase (ALP), and gamma-glutamyl transferase (GGT)], inflammatory cytokines [monocyte chemoattractant protein-1 (MCP-1/CCL2) and interleukin 6 (IL-6)], and hormones (insulin, leptin, and active ghrelin). Gut microbial profiling was performed to assess compositional changes. The CAF offspring exhibited higher levels of serum glucose, insulin, TGs, MCP-1, and IL-6 compared with the control group. Moreover, the CAF diet altered the intestinal bacterial community structure, increasing the abundance of Prevotellaceae and Lachnospiraceae while reducing Lactobacillaceae. Our results suggest that ingesting a CAF diet during maternal programming promotes adverse impacts on the offspring metabolism homeostasis, inflammatory responses, and intestinal microbiota composition.
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