Brown adipose tissue (BAT) has been described in various mammals since 1551, but it is only over the last century that it has become clear that this tissue exists in all mammals. The realisation that heat production is a major function of BAT, was the result of studies in the 1970s that described regulated uncoupling of oxidative phosphorylation in BAT mitochondria and demonstrated that the mechanism for this uncoupling was the existence of a unique protein (UCP1) expressed only in BAT that could dissipate the electrochemical gradient across the inner mitochondrial membrane. Other studies in the 1980s showed that BAT was an insulin sensitive tissue with a large capacity for glucose utilisation, lipogenesis, fatty acid utilisation and oxygen consumption (1). The potential impact of uncoupled BAT activity on substrate oxidation without energy conservation led to a concerted research effort to discover compounds to increase the amount of BAT and to activate BAT as a mechanism for increasing energy expenditure and treating obesity. However, lead compounds in animal studies did not translate to effects in humans leading to idea that BAT was not an anti-obesity target tissue in humans (2). The recent “re-discovery” of BAT in humans and the demonstration that white adipose tissue may be transformable, at least to some extent, into adipose tissue capable of carrying out uncoupled respiration, has re-invigorated the idea of harnessing BAT to regulate energy balance (3). Despite the potential however, major questions remain regarding how much BAT exists in humans and to what extent can activated BAT or activated “beige” fat contribute to whole body substrate oxidation and energy expenditure and therefore significantly whole body energy metabolism.