Adrenaline and noradrenaline, the main effectors of the sympathetic nervous system and adrenal medulla, respectively, are thought to control adiposity and energy balance through several mechanisms. They promote catabolism of triglycerides and glycogen¹, stimulate food intake when injected into the central nervous system², activate thermogenesis in brown adipose tissue^3,4, and regulate heat loss through modulation of peripheral vasoconstriction and piloerection¹. Thermogenesis in brown adipose tissue occurs in response to cold and overeating (diet induced)^5-7, and there is an inverse relationship between diet-induced thermogenesis and obesity both in humans⁸ and in animal models^9-12 . As a potential model for obesity, we generated mice that cannot synthesize noradrenaline or adrenaline by inactivating the gene that encodes dopamine β-hydroxylase. These mice are cold intolerant because they have impaired peripheral vasoconstriction and are unable to induce thermogenesis in brown adipose tissue through uncoupling protein (UCP1). The mutants have increased food intake but do not become obese because their basal metabolic rate is also elevated. The unexpected increase in basal metabolic rate is not due to hyperthyroidism, compensation by the widely expressed uncoupling protein UCP2, or shivering.