The effect of insulin hypoglycaemia on serum gastrin and gastric acid in normal subjects and patients with duodenal ulcer.

Abstract

Abstract Serum gastrin was measured by radio-immuno-assay in normal subjects and in patients with duodenal ulcer during insulin hypoglycaemia with and without concomitant aspiration of gastric acid. Insulin hypoglycaemia alone caused a rise in serum gastrin from 8.0 to 45.0 pg. per ml. in patients with duodenal ulcer, which was significantly greater than the rise from 13.0 to 29.0 pg. per ml. in normal subjects. During gastric aspiration serum-gastrin levels remained elevated for longer periods. The maximum increase of serum gastrin after insulin during gastric aspiration provided an almost complete discrimination between patients with duodenal ulcer and normal subjects. This discrimination between the groups was complete when serum gastrin was measured during insulin hypoglycaemia combined with intragastric neutralization of acid. The timing of the peak serum gastrin and the lowest blood-glucose coincided, but the peak acid output occurred 15–30 minutes later. Serum gastrin was inversely correlated with blood-glucose. Blood-glucose decreased to significantly lower levels in unaspirated than in aspirated subjects. These studies suggest that patients with duodenal ulcer produce more gastrin than normal subjects in response to insulin hypoglycaemia (and, by inference, to vagal stimulation). The results support the concept of an increased functional G-cell mass in duodenal ulcer patients, and indicate the physiological roles of vagally released gastrin and of the acid inhibitory mechanism. Discriminant functions observed in the study could form the basis of tests for the presence of the duodenal ulcer diathesis.