In order to help define the sequential neural, humoral and metabolic responses to feeding, an experimental model involving refeeding 3-day fasted rats a single meal has been developed. The post-prandial rise in resting oxygen consumption is taken as the metabolic end-point, but unlike the response in animals fed normally, shows a marked (24 h) delay. Using a variety of pharmacological and endocrinological techniques it has been possible to show that the delay results from a complex sequence of events involving changes in blood glucose, insulin, thyroid hormones, sympathetic activity and brown fat. The possible role of the ventomedial hypothalamus in mediating some of these events is discussed and the failure of genetically obese rats to exhibit a postprandial rise in oxygen consumption is ascribed to insulin-insensitivity.