Defective BAT thermogenesis is associated with obesity in all the different types of obese animal so far studied. The deficit in normal energy expenditure may be presumed to contribute to the high metabolic efficiency and, together with the hyperphagia, to the obesity of these animals. In two types of obese animal (the ob/ob mouse, the db/db mouse) an increased propensity to become torpid provides an additional energy conserving mechanism that contributes to the high metabolic efficiency. In all these animals an abnormality of hypothalamic function appears likely. Obviously animals with induced hypothalamic lesions (the VMH-lesioned rat, the GTG-obese mouse) have an interruption in the normal pathway that links diet and the sympathetic innervation of BAT. The fa/fa rat resembles these animals in failing to activate BAT thermogenesis in response to diet: the lesion may lie in the hypothalamus itself or elsewhere in the food-intestine-hypothalamus-BAT axis, for example in intestinal peptide hormones. The ob/ob mouse has a peculiar hypothalamic defect that interferes with control of thermogenesis in BAT as well as impairing or exaggerating some aspects of thermoregulation. The db/db mouse resembles the ob/ob mouse but, since the defect is genetically distinct, presumably has a different lesion at the molecular level.