It is well established that electrical stimulation of the ventromedial hypothalamus (VMH) causes a reduction in food intake, whereas electrolytic or chemical lesions in this area result in hyperphagia and obesity in the rat. This has led to the suggestion that either the ventromedial nucleus itself, or nerve fibres passing close by, are important in the control of food intake. However, obesity due to VMH lesions occurs in weanling rats in the absence of hyperphagia and can develop in adult rats pair-fed with controls, indicating that destruction of this area also causes an increased metabolic efficiency (that is, a reduced energy expenditure). In normal rats, hyperphagia induced by feeding a highly palatable cafeteria diet is often accompanied by a large increase in heat production (diet-induced thermogenesis) which tends to prevent excessive weight gain and obesity. This diet-induced thermogenesis is due to sympathetic activation of brown adipose tissue (BAT) and we have now investigated the possibility that the VMH is involved in the activation of this process. We found that electrical stimulation of this area produced increased BAT thermogenesis, which suggests that the VMH exerts a dual influence in the regulation of energy balance--an inhibitory effect on energy intake and a stimulatory effect on thermogenesis and energy output.