2003 Volume 56 Issue 1 Pages 33-39
Brown adipose tissue (BAT) is the major site for metabolic heat production during spontaneous hyperphagia as well as cold acclimation. Thermogenesis in BAT, which is associated with activation of glucose and fatty acid metabolism in the tissue, is under direct control of the sympathetic nervous system. Although the ventromedial hypothalamus (VMH) is widely accepted to be a satiety center, it also involves a sympathetic neural component. In fact, BAT thermogenesis is enhanced and impaired by stimulation and lesioning of the VMH, respectively. Since BAT thermogenesis is a significant component of whole-body energy expenditure, at least in small rodents, obesity observed after VMH lesioning is attributable not only to increased food intake but also to decreased BAT thermogenesis. Sympathetic activation of BAT thermogenesis is mediated through the β-adrenergic action of norepinephrine released from the nerve endings. Some agonists of the β3-adrenergic receptor, which is expressed exclusively in adipocytes, activate BAT thermogenesis and lipid mobilization from white adipose tissue, and finally reduce adipocity. Moreover, hyperphagia-induced and sympathetically mediated BAT thermogenesis is attenuated by gastric tube feeding, suggesting a role of afferent input from oro-pharyngeal receptors. Thus, food-associated sensory factors such as taste, in addition to food energy content itself, are significantly involved in the regulation of energy expenditure.
