Obesity is defined as excess fat accumulation in white adipose tissue. In opposition to this storage function, brown adipose tissue (BAT) counters obesity, by consuming fat through thermogenesis. Obese individuals display lower BAT mitochondrial oxidative capacity and altered mitochondrial morphology. A promising strategy to fight obesity is dietary polyphenols, which increase BAT mass and function, stimulating energy expenditure (EE). Calafate, a polyphenol-rich Chilean native fruit, has anti-inflammatory and antioxidant characteristics. The effect of a Calafate extract (50 mg [total polyphenols]/kg body weight/day) on EE and mitochondrial function and morphology in BAT from obese mice was assessed. Adult male C57BL/6J mice were subdivided into four treatments for 18 weeks: control diet (C), control diet + Calafate (CC), high-fat diet (HF), high-fat diet + Calafate (HFC). Calafate extract decreased high-fat diet-induced body weight gain from week 6 of treatment (p<0,05) and increased EE at rest (p = 0.03). In BAT, Calafate extract reversed the decrease in UCP-1 protein levels generated by the high-fat diet (p = 0.004). Also, Calafate extract improved mitochondrial transmembrane potential (p = 0.04). The extract did not substantially modify mitochondrial morphology, although it increased the expression of optic atrophy protein 1 (p = 0.01), a mitochondrial fusion-related protein. In sum, consumption of a polyphenol-rich Calafate extract prevents high-fat diet-induced obesity, concomitant with higher energy expenditure, and improved BAT mitochondrial function in obese mice.
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