Abstract / Summary
White adipose tissue dysfunction is a central event in the development of obesity-associated metabolic disorders. Kumquat (Fortunella japonica) is consumed whole, allowing intake of peel-derived bioactive compounds. Although increasing evidence suggests that kumquat exerts beneficial metabolic effects, its impact on white adipose tissue homeostasis remains poorly understood. We investigated whether chronic supplementation with lyophilized whole kumquat could attenuate adipose tissue dysfunction in high-fat diet (HFD)-fed mice. Male C57BL/6J mice received a standard diet, HFD, or HFD supplemented with 5% (w/w) kumquat (HFD + K) for 24 weeks. Kumquat attenuated body weight gain, reduced food intake and caloric efficiency, and decreased epididymal white adipose tissue mass. Histological analysis showed reduced adipocyte hypertrophy and a shift toward smaller adipocytes. Kumquat also decreased macrophage crown-like structures and Tnf and Il1b expression, while increasing circulating adiponectin, lowering leptin, and improving the leptin/adiponectin ratio. At the molecular level, kumquat increased Pparg, Ppargc1a, Sirt1, Cox4i1, and Ucp1 expression, together with mitochondrial DNA copy number, consistent with changes in molecular markers associated with mitochondrial remodelling and thermogenic pathways. Overall, these findings identify white adipose tissue as a relevant target of chronic whole-kumquat consumption during diet-induced obesity and suggest that preservation of adipose tissue homeostasis involves coordinated anti-inflammatory, endocrine, and mitochondrial-related molecular adaptations.