Adaptive adrenergic thermogenesis is induced in two physiological conditions. One form develops as an effect of acclimation to cold ("classical nonshivering thermogenesis"); the other (the existence of which is still somewhat controversial) develops as an effect of the intake of certain diets (e.g. "cafeteria diet"). Thermogenesis in brown adipose tissue is fully dependent on the activity of uncoupling protein 1 (UCP1). Thus, the importance of brown adipose function for different forms of thermogenesis can be established in UCP1-ablated mice. In the absence of UCP1, classical thermoregulatory nonshivering thermogenesis is fully obliterated - but the animals can compensate for the absence of nonshivering thermogenesis by shivering. Upon exposure to a palatable diet, the mice without UCP1 have no alternative to the metaboloregulatory thermogenesis occurring in brown adipose tissue, and they will therefore become obese. The present realization that brown adipose tissue is present and active even in adult humans raises evidently questions as to the significance of brown-fat thermogenesis in the protection against obesity (as well as against diabetes) and opens new possibilities for development of therapeutic agents against obesity and the metabolic syndrome in general.