Cold exposure stimulates heat production by means of shivering, an inv
oluntary contraction of skeletal muscle, as well as thermoregulatory n
onshivering 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 w
as definitely described by Cannon et al. [1] in 1927, who claimed a si
gnificant role of adrenal medulla in NST. It has been now established
by a number of studies that metabolic acclimation to cold is character
ized 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 ti
ssue (BAT), which is solely differentiated for thermogenesis and the o
nly 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 metabo
lic activity of BAT, but also markedly proliferate this tissue. The ex
tent of hyperplasia in BAT is greater than in any other tissues or org
ans under various physiological stimuli. It is surmised that such feat
ures of BAT are under the control of multiple neuroendocrine factors.
However, the mechanisms involved have not been fully elucidated. We ha
ve been concerned with the conditions and the factors which cause the
activation of BAT. The present minireview will focus on some factors d
irectly affecting BAT mainly on the basis of studies in our laboratory
.