HYPOTHALAMIC REGULATION OF ENERGY-BALANCE AND FEEDING-BEHAVIOR (REPRINTED FROM FEDERATION-PROC, VOL 33, PG 1150-1165, 1974)

Brain damage localized to the ventromedial hypothalamus (VMH) can produce overeating and obesity, However, because of several other behavioral symptoms, namely finickiness and laziness, the VMH mediation of short-term satiety has long been in doubt. A solution to this ''VMH paradox'' is proposed. Feeding behavior of normal animals is controlled by two concurrent processes-one reflecting short-term satiety and the other, long-term regulation of feeding. The VMH is proposed to mediate the second process. In other words, neurons within the VMH stimulate appetite when body nutrient stores are low and reduce appetite when body nutrient stores are high. Destruction of the excitatory component explains Lack of motivation in lesioned animals when confronted by appetite deterrents. Experimental evidence for the conclusion consists primarily of lesioned animals' failure to exhibit compensatory food intake when deprived of Toed or treated with insulin. It is further proposed that long-term regulatory control of food intake is organized around an anabolic intermediary of glucose stored within specialized cells of the medial hypothalamus. In support of this idea, it is shown I) the VMH retains C-14 for longer periods than the rest of the brain after radioactive glucose loads; 2) daily food intake can be inhibited by direct administration of glucose into the VMH; 3) when retention of carbon within the VMH is decreased, the satiating capacity of glucose is reduced; d) manipulations which increase incorporation of carbon into the VMH increase satiety. Preliminary evidence indicates that the C-14: in the VMH has been incorporated into a lipid fraction to a greater extent than in the lateral hypothalamus. Literature relevant to hypothalamic integration of feeding is reviewed. -PAN KSEPP, J. Hypothalamic regulation of energy balance and feeding behavior.