Hypothalamic control of food intake in cats and monkeys

Abstract

The role of the central nervous system in regulating food intake was probably suggested first by the discovery that either obesity or emaciation may occur in patients with nervous diseases. For a while these observations were not properly evaluated, because emphasis was laid upon the obesity as such, or the leanness, rather than upon the changed eating habits responsible for the clinical picture. Interest was focused on the hypothalamic region by the experimental studies of many workers (Hetherington, 1941; Hetherington & Ranson, 1940, 1942 a, b; Brobeck, Tepperman & Long, 1943; Kennedy, 1950; Ranson, Fisher & Ingram, 1938) who showed that bilateral lesions in the medial hypothalamus, especially lesions in or ventro-lateral to the ventromedial nucleus, resulted in obesity. The confusion introduced by the notion that pituitary disturbances caused obesity was also clarified by Hetherington (1943), who showed that the hypophysis is in no way directly concerned with the pathogenesis of obesity following injury to the base of brain. Brobeck et al. (1943) demonstrated that this hypothalamic obesity was due to increased food intake (hypothalamic hyperphagia) rather than to disturbances in the fat, carbohydrate or intermediary metabolism. From the time of its discovery this hyperphagia was assumed to be a release phenomenon brought about through the destruction of an inhibitory mechanism.The existence of another mechanism in the lateral hypothalamus of the rat, which controls the 'instinct' or the 'urge' to eat, was demonstrated by Anand & Brobeck (1951 a, b). They showed that bilateral destruction of a well localized area in the lateral hypothalamus, at the same rostro-caudal level as the ventro-medial nucleus, produces complete aphagia and death due to starvation, in spite of the availability of food. It was also observed that of the two mechanisms the lateral one exerts the more basic type of control over food intake and the medial one (inhibitory) produces its effects only when the lateral is intact. The lateral mechanism is designated a 'feeding centre', or even an 'appetite centre', while the medial one is called a 'satiety centre'. Joliffe named the two, together, the 'appestat'. The present study was undertaken to determine, whether similar mechanisms exist in the hypothalamic regions of higher mammals, cats and monkeys, and also whether they are modified by the more highly evolved higher nervous centres.