Brown adipose tissue (BAT), an organ specialized in the conversion of chemical energy from nutrients into heat through a process denominated as nonshivering thermogenesis, plays an important role in defence of body weight and homoeothermy in mammals. BAT nonshivering thermogenesis relies on the activity of the uncoupling protein 1 (UCP-1), a mitochondrial protein that, on demand, deviates proton gradient from ATP synthesis to heat generation. Energetically, this process is supported by BAT-elevated mitochondrial density and outstanding capacity to oxidize fatty acids and glucose. These unique features place BAT as an important determinant of whole-body energy, lipid and glucose homoeostases. In the present issue of Clinical Science, Poekes et al. have gathered supporting evidence indicating that, along with hyperphagia, impaired BAT diet-induced thermogenesis is an important factor driving the exacerbated diet-induced obesity, glucose intolerance and hepatic steatosis featured by foz/foz, a mouse strain that carries mutations in Alström syndrome protein 1 (ALMS1) gene mimicking human Alström syndrome. They also show that restoration of BAT nonshivering thermogenesis by intermittent cold exposure attenuated foz/foz mice obesity, glucose intolerance and liver steatosis. Altogether, these findings highlight the important contribution of BAT nonshivering thermogenesis to whole-body energy expenditure, lipid and glucose homoeostases and further support its potential utilization as a therapeutic strategy to treat metabolic diseases.

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