A Thermally Processed Cafeteria Diet Reproducibly Mimics Early Metabolic Syndrome Through Obesogenic, Inflammatory, and Adipose Dysfunctions in Wistar Rats.

The obesogenic nutrient composition and processing characteristics of ultra-processed foods may contribute to metabolic dysfunction. This study evaluated a standardized cafeteria diet, alone or combined with low-dose streptozotocin (STZ), in male Wistar rats. Animals (n = 32) were allocated to Healthy Control, STZ (35 mg/kg), Cafeteria Diet (CAF), and CAF+STZ groups. The diet contained standard chow, condensed milk, refined sugar, hydrogenated fat, soybean oil, and chocolate-filled biscuits, homogenized and thermally processed at 180 °C. After 102 days, anthropometric, metabolic, inflammatory, gene expression, microbiota, and histopathological parameters were assessed. CAF induced a marked obesogenic phenotype, with increased body weight (+172.3%) and abdominal circumference (+38.7%; p < 0.01). CAF showed hyperglycemia (median glucose, 403 mg/dL) and higher HOMA-IR than Healthy Control (p < 0.01); CAF+STZ also showed increased HOMA-IR (p < 0.05). CAF increased IL-1β and IL-6 (p < 0.05), triglycerides, adipocyte hypertrophy (p < 0.01), and adipose Leptin expression (p < 0.05), while reducing muscle Slc2a4/GLUT4 expression (p < 0.01). Liver, kidney, and pancreatic histopathological scores did not differ significantly. Gut microbiota showed marked compositional imbalance and low taxonomic evenness, with Firmicutes (99.83%), Ligilactobacillus (99.36%), and Lactobacillaceae (99.52%) predominating, while Enterobacteriaceae represented 0.14%. Despite no reduction in Shannon or Simpson indices, extreme Ligilactobacillus dominance indicated a restricted and uneven community. Overall, the cafeteria diet reproduced obesity-associated metabolic dysfunction, characterized by hyperglycemia, insulin resistance, inflammation, adipocyte hypertrophy, altered glucose and leptin expression, and substantial microbiota restructuring.