The endocrinological and biochemical mechanisms controlling energy expenditure in brown adipose tissue at the cellular as well as at the total tissue levels are briefly reviewed. Thermogenesis in brown adipose tissue is principally controlled by the activity of hormone-sensitive lipases that represent the 'flux-generating' step in the stimulus-calorigenesis sequence. Long chain fatty acids are the physiological messengers regulating mitochondrial respiration. Agents stimulating brown adipocyte lipolysis (catecholamines, glucagon, methylxanthines) also stimulate respiration, and conversely, agents inhibiting lipolysis (adrenergic antagonists, insulin, prostaglandins) also inhibit respiration. This indicates that lipolysis and respiration are functionally coupled in brown adipose tissue. On the other hand, brown adipose tissue thermogenic capacity increases during cold acclimation or adaptation to hyperphagia. Brown adipocyte proliferation and differentiation from precursor cells (interstitial cells and brown preadipocytes) represent the fundamental phenomena explaining the increase capacity of cold acclimated and/or hyperphagic animals for responding calorigenically to catecholamines. Physiological situations associated with a stimulation of energy expenditure and a negative energy balance (cold acclimation, exercise training, caffeine consumption) generally induce a stimulation of adipocyte proliferation in brown adipose tissue that is accompanied by a simultaneous inhibition of cell proliferation in white adipose tissue. The physiological significance of these metabolic adaptations is to modulate the capacity of homeothermic animals for energy expenditure in accordance with energy requirements.