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Brown adipose tissue (BAT) is an organ specialized to fuel nonshivering thermogenesis for the defense of high body temperature of many eutherian mammals in the cold. Cold-induced sympathetic stimulation of brown adipocytes activates lipolysis, glucose uptake, and mitochondrial biogenesis, with the mitochondrial biogenesis providing a powerful cellular engine for heat generation. At the mitochondrial inner membrane, the energy of nutrients such as glucose and lipids is converted into a proton gradient, but instead of storing the potential energy in the generation of ATP, uncoupling protein 1 (UCP1) catalyzes an inducible proton leak to release the energy of the proton gradient directly as heat. The central role of UCP1 for nonshivering thermogenesis in rodents has been confirmed in knockout mice (1, 2), and the majority of research efforts on BAT and UCP1 centers on the physiological consequences of thermogenesis, including the regulation of body weight for treatment of obesity and other metabolic diseases. Although it appears that UCP1’s function to release the proton motive force as the final energy conversion step may only affect thermogenesis, reduction of the proton motive force will inevitably impact other mitochondrial and cellular processes. Reducing proton motive force by mitochondrial proton leak would alter the redox state of the respiratory chain and potentially reduce the production of reactive oxygen species (ROS) (3). The absence of UCP1 in BAT could be problematic, given the high concentration of respiratory chain complexes in cold-acclimated brown fat mitochondria and the minor concentrations of ATP synthase, with the latter not being able to release the enhanced, cold-induced proton motive force. Although the physiological consequences in UCP1 knockout mice have been almost exclusively attributed to thermogenesis, there may be further consequences on mitochondrial ROS biology and downstream effects that have been widely ignored. In PNAS, Kazak et al. (4) explore cold-induced …

Uncoupling protein 1 controls reactive oxygen species in brown adipose tissue