The role of glucose in insulin-induced feeding and drinking☆

Abstract

The greater the dose of insulin given in a single injection the deeper the induced hypoglycaemia, whereas over the same dose range the amount of eating elicited comes to a maximum and then declines. The maximum rate of insulin-induced drinking occurs during rapid fall in blood glucose concentration but the induced eating coincides with a period of relatively constant blood glucose concentration. Injection of concentrated glucose with the insulin delays the induction of feeding, but co-injection of approximately isotonic glucose gives shorter feeding latencies than co-injection of more dilute solutions. Glucose ingestion at the time of insulin injection, but not before or after, eliminates induced feeding. Gastric intubation of glucose can block both eating and drinking responses to insulin. Unmetabolizable 3-methylglucose is not so effective at blocking the eating. Glycerol diminishes and intragastric palmitate augments the induced feeding. It is suggested that elicitation of eating by injected insulin is mediated by metabolic signals generated by adaptation to changed body glucose distribution.