Food consumption, plasma glucose and stomach-emptying in insulin-injected hamsters.

Two experiments were performed to investigate whether insulin-induced hyperphagia (IIH) serves an adaptive function in counteracting hypoglycemia in hamsters. In Experiment 1, insulin-injected hamsters having free access to food during a six-hour feeding test had neither higher plasma glucose (PG) concentrations nor lower frequencies of neurological impairment at the end of the test than did hamsters whose food intake was restricted to control levels. In Experiment 2, it was observed that PG fluctuations did not act as a trigger for meal-onset in insulin-injected hamsters, nor was PG affected by consumption of a meal during IIH. The withholding of food for periods longer than the typical intermeal interval (IMI) of insulin-injected hamsters (= 50 min) resulted in a marked increase in the frequency of neurological deficits among hamsters having PG levels lower than about 40 mg/dl. However animals with similarly low PG concentrations, but deprived of food for less than 50 min showed no signs of impairment, suggesting that some alternate metabolic fuel is available during the IMI and prevents the occurrence of behavioural deficits. The results of these experiments suggest that a simple glucostatic interpretation of IIH in hamsters is inadequate, and although hyploglycemia may play a role in hamster IIH, other factors must also be considered. In Experiment 3, the effect of a hyperphagia-inducing dose of insulin upon stomach emptying was investigated. It was found that both insulin-injected and control hamsters have similar amounts of food in their respective pregastric and gastric pouches at both the onset and offset of meals, but that both pouches empty far more rapidly under the influence of insulin.(ABSTRACT TRUNCATED AT 250 WORDS)