Metabolic and neurochemical correlates of glucoprivic feeding

Abstract

Various hypotheses are reviewed concerning the mechanisms of feeding induced by insulin or 2DG. New data are presented to show that elevated plasma ketone levels are not sufficient to suppress 2DG feeding, suggesting that nourishment of the brain either does not occur or is not sufficient to stop 2DG feeding. We find that both acetoacetate and hydroxybutyrate suppress spontaneous feeding. Another series of studies investigated the effects of 2DG and insulin on catecholamine turnover in several brain regions of animals that do (rat, mouse) or do not (hamster) eat in response to these stimuli. The effects of glucoprivic stimuli on NE turnover were minimal; however, 2DG did appear to inhibit DA turnover, especially in nucleus accumbens. Thus, brain NE does not seem specifically involved in glucoprivic feeding, data which are supported by a lack of additivity of feeding induced by 2DG and by clonidine. Finally, to resolve some of the disparate data concerning the effects of glucose infusion on insulin-induced feeding, we examined the time course for effects on feeding and for glucose tolerance. It appears that glucose strongly inhibits feeding only when it is utilized.