Bergamot (Citrus bergamia) preserves cardiac structure and function and modulates myocardial redox and metabolic profiles in diet-induced obesity.

Obesity promotes cardiac remodeling and dysfunction through oxidative stress, inflammation, and metabolic disturbances. Citrus bergamia (bergamot) has shown beneficial effects on obesity-related cardiometabolic risk factors, but its cardiac effects remain unclear. We evaluated bergamot supplementation in a rat model of diet-induced obesity using integrated assessments of cardiac structure and function, redox and inflammatory status, biogenic amines, fatty acids, and metabolites. Wistar rats (n = 54) were randomized to Control, Obese, or Obese + Bergamot groups for 20 weeks; bergamot was administered by gavage at 250 mg/kg/day. Animals in both obese groups had higher body weight (p < .01) and adiposity index (p < .0001) than controls, confirming diet-induced obesity. Untreated obese rats also exhibited higher systolic blood pressure, cardiac remodeling, oxidative damage, higher cardiac TNF-α and IL-10 concentrations, and reduced NRF2 expression (p < .05). Bergamot attenuated cardiac remodeling, preserved systolic and diastolic function (p < .05), reduced malondialdehyde (p < .05), protein carbonyls (p < .0001), and cardiac TNF-α and IL-10 concentrations (p < .05), and increased ferric reducing antioxidant power (p < .01). Exploratory cardiac metabolic profiling showed partial recovery of putrescine and spermidine, higher spermine and histamine concentrations (p < .05), lower serotonin monoforms (p < .05), higher arachidonic acid abundance (C20:4n6; p < .05), and higher inosine abundance (p < .05) following bergamot supplementation. Bergamot-associated cardiac preservation occurred despite persistent obesity and without restoration of NRF2 expression, the NRF2/KEAP1 ratio, or myocardial NAD+ and NADP+ concentrations. Changes in polyamine, fatty acid, and purine-related profiles, including higher spermine and inosine, identify candidate metabolic features associated with this response but do not establish these metabolites as causal mediators.