Brown adipose tissue is uniquely able to rapidly produce large amounts of heat through activation of uncoupling protein (UCP) 1. Maximally stimulated brown fat can produce 300？watts/kg of heat compared to 1？watt/kg in all other tissues. UCP1 is only present in small amounts in the fetus and in precocious mammals, such as sheep and humans; it is rapidly activated around the time of birth following the substantial rise in endocrine stimulatory factors. Brown adipose tissue is then lost and/or replaced with white adipose tissue with age but may still contain small depots of beige adipocytes that have the potential to be reactivated. In humans brown adipose tissue is retained into adulthood, retains the capacity to have a significant role in energy balance, and is currently a primary target organ in obesity prevention strategies. Thermogenesis in brown fat humans is environmentally regulated and can be stimulated by cold exposure and diet, responses that may be further modulated by photoperiod. Increased understanding of the primary factors that regulate both the appearance and the disappearance of UCP1 in early life may therefore enable sustainable strategies in order to prevent excess white adipose tissue deposition through the life cycle. 1. Introduction The study of brown adipose tissue (BAT) biology has always been an exciting and vibrant arena not least because although this tissue is present in comparatively small amounts, it can have a pivotal role in energy balance [1, 2]. BAT is characterised as possessing large amounts of the unique uncoupling protein (UCP) 1 which when activated enables the free-flow of protons across the inner mitochondrial membrane, resulting in the rapid dissipation of chemical energy as heat [1]. Consequently, when maximally activated, BAT can generate up to 300？W/kg of tissue compared with 1？W/kg from most other tissues [3]. This process is regulated primarily by the unmasking of GDP-binding sites located within UCP1 [4, 5] and represents the initial response necessary to ensure rapid heat generation [6]. The primary energy source for this process comes from nonesterified fatty acids that are released from lipid at the same time as UCP1 is activated, usually through activation of the sympathetic nervous system [1]. Despite the control of BAT being well documented from a range of investigations in both small [7] and large mammals [8], it has only been over the past decade following the discovery of the presence of thermogenically active BAT in adult humans that its potential role in a range of homeorhetic processes has been
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