Abstract
Brown adipose tissue (BAT) represents a remarkable heat-producing tissue. The thermogenic potential of BAT is conferred by uncoupling protein 1, a protein found uniquely in brown adipocytes. BAT activity and capacity is controlled by the sympathetic nervous system (SNS), which densely innervates brown fat depots. SNS-mediated BAT thermogenesis is essentially governed by hypothalamic and brainstem neurons. BAT activity is also modulated by brain energy balance pathways including the very significant brain melanocortin system, suggesting a genuine involvement of SNS-mediated BAT thermogenesis in energy homeostasis. The use of positron emission tomography/computed tomography scanning has revealed the presence of well-defined BAT depots in the cervical, clavicular, and paraspinal areas in adult humans. The prevalence of these depots is higher in subjects exposed to low temperature and is also higher in women compared to men. Moreover, the prevalence of BAT decreases with age and body fat mass, suggesting that BAT could be involved in energy balance regulation and obesity in humans. This short review summarizes recent progress made in our understanding of the control of SNS-mediated BAT thermogenesis and of the determinants of BAT prevalence or detection in humans.
Highlights
Brown adipose tissue (BAT) is a specialized tissue whose main function is to produce heat
One such system includes the brain metabolic melanocortin system, which acts via the activation of melanocortin-4 receptor (MC4R), thereby controlling energy expenditure while enhancing BAT thermogenesis (Ste et al, 2000; Butler, 2006)
Numerous brain populations of MC4R mRNA-harboring neurons that are synaptically connected to BAT (Song et al, 2008) and white adipose tissue (WAT) (Song et al, 2005) have been identified
Summary
Brown adipose tissue (BAT) is a specialized tissue whose main function is to produce heat. The SNS activity in BAT is governed by the brain autonomic centers including hypothalamus and brainstem, which are regions involved in the cold-induced thermogenesis (Morrison, 2011) and energy balance regulation (Richard, 2007; Richard and Picard, 2011).
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