Dietary selenate attenuates adiposity and improves insulin sensitivity in high-fat diet-induced obese mice

Abstract Selenium is an essential micronutrient required for maintaining cellular redox homeostasis. Despite its potential beneficial role in lowering the risk of type 2 diabetes in humans with lower selenium status and diabetic mice, its role in preventing the development of obesity and metabolic syndrome is unknown. Here, we report that chronic selenate supplementation to high fat (HF) diet-fed mice resulted in resistance to diet-induced adiposity and insulin resistance. The body weight and adipose tissue mass gain associated with HF diet-induced obesity in mice was abrogated by selenate supplementation at 0.72 mg/kg body weight. This was accompanied by alteration of HF diet-induced expression of genes involved in adipokines, inflammation, transforming growth factor-β (TGF-β) signalling, mitochondria function, and beige adipocyte differentiation in adipose tissue. Selenate supplementation also resulted in an increase in faecal calorie content and improved glucose tolerance in HF diet-induced obese mice. Collectively this study elucidated a novel role of selenate as a dietary micromineral in the prevention of obesity and its related energy dysfunction.