BROWN ADIPOSE-TISSUE THERMOGENESIS AS PHYSIOLOGICAL STRATEGY FOR ADAPTATION

Cold exposure stimulates heat production by means of shivering, an involuntary contraction of skeletal muscle, as well as thermoregulatory nonshivering thermogenesis (NST). Although chemical regulation of heat production without muscular movement, NST, was first suggested by the observation of Voit in 1878 (see Ref. [1]), occurrence of NST in man was definitely described by Cannon et al. [1] in 1927, who claimed a significant role of adrenal medulla in NST. It has been now established by a number of studies that metabolic acclimation to cold is characterized by an enhanced NST as a more efficient means of heat acquisition than shivering and the major site for NST is a unique brown adipose tissue (BAT), which is solely differentiated for thermogenesis and the only known tissue whose main function is heat production. Many reviews have been written on the biochemical and physiological mechanisms for NST and BAT functions [2-4]. Cold acclimation enhances not only metabolic activity of BAT, but also markedly proliferate this tissue. The extent of hyperplasia in BAT is greater than in any other tissues or organs under various physiological stimuli. It is surmised that such features of BAT are under the control of multiple neuroendocrine factors. However, the mechanisms involved have not been fully elucidated. We have been concerned with the conditions and the factors which cause the activation of BAT. The present minireview will focus on some factors directly affecting BAT mainly on the basis of studies in our laboratory.