The young rat adjusts its food intake so precisely to its energy needs that its fat stores remain almost constant. Considerable variation in food intake is brought about in response to change in heat loss to the environment, or in loss of food through the mammary gland in lactation, without appreciable change of weight. Hypothalamic damage permits excessive intake and causes obesity. The degree of obesity and in general its rate of development, is a function of the degree of damage to the region of the tuber cinereum, and is independent of changes of intake with environmental temperature. It is suggested that the hypothalamic satiety mechanism is concerned only in the prevention of an overall surplus of energy intake over expenditure, which would cause the deposition of fat in the depots. The simplest way in which this lipostasis could be achieved is by sensitivity to the concentration of circulating metabolites. There is no disturbance of temperature regulation or acclimatization to changed environmental temperature in obese rats. These findings do not support the suggestion made by Brobeck (1946) that food intake is controlled as part of the normal regulation of body temperature by a thermosensitive hypothalamic centre. The maximum daily intake of food during hyperphagia appears to be determined by some limiting factor additional to the hypothalamic mechanism. A similar factor appears to operate in lactation. Reasons are advanced for regarding this as the limiting rate at which absorbed foodstuffs can be removed from the circulation, that is as some aspect of the synthesis or transport of fat.