Behavioral, neuroanatomic, and neuroinflammatory characteristics of metabolic syndrome in cafeteria diet-induced obese male rats.

Authors

Andrej Feješ, Jakub Szabó, Petronela Sušienková, Ladislav Bačiak, Lucia Mihalovičová, Veronika Kunšteková, Veronika Borbélyová, Katarína Šebeková

Published in

Metabolic brain disease. Volume 41. Issue 1. Sep 23, 2026. Epub Sep 23, 2026.

Abstract

Obesity and metabolic syndrome are associated with low-grade systemic inflammation and neuroinflammation, potentially contributing to structural brain alterations and cognitive decline. This study evaluated brain volumetry, metabolic disturbances, neuroinflammation markers, and behavioral outcomes in a rat model of diet-induced obesity. Male Wistar rats were fed either a standard diet (CTRL; n = 6) or a cafeteria diet (CAF; n = 6) for five months from weaning. Metabolic parameters (weight, glucose tolerance, blood pressure, lipids), behavior (Open Field, Novel Object Recognition), and brain regional volumes (4.7 T MRI) were assessed. Neuroinflammatory markers (tumor necrosis factor-α levels (TNF-α) and glial fibrillary acidic protein (GFAP)) were quantified in the hypothalamus and olfactory bulb. CAF rats developed a metabolic syndrome-like phenotype characterized by abdominal adiposity, insulin resistance, hypertension, and dyslipidemia (p < 0.05). They also showed higher hypothalamic GFAP and TNF-α levels, higher relative orbitofrontal cortex volume (p < 0.05) than controls, whereas lower relative hypothalamic and corpus callosum volumes did not reach significance. Behaviorally, CAF rats exhibited reduced locomotor activity, impaired short-term memory, and higher grooming activity (p < 0.05). Multivariate modeling identified hypothalamic neuroinflammation, severity of continuous metabolic syndrome z-score, and reduced corpus callosum volume as key predictors of cognitive and behavioral impairments. Long-term consumption of a CAF diet induces key features of human metabolic syndrome, hypothalamic neuroinflammation, region-specific brain volumetric alterations, and cognitive deficits. These findings support a role for the metabolic-inflammatory axis in brain vulnerability and suggest that preservation of neuroimmune homeostasis may be important for maintaining cognitive health in obesity-associated metabolic disorders.

PMID:
42776316
Bibliographic data and abstract were imported from PubMed on 24 Sep 2026.

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