The evidence for the regulatory role of endogenous GIP as a glucose dependent insulinotropic hormone in patients with duodenal ulcer.

In order to investigate the mechanism of GIP secretion and the role of endogenous GIP in the enteroinsular axis in duodenal ulcer patients, we have compared plasma GIP, insulin, and blood glucose responses to oral glucose ingestion in 10 duodenal ulcer patients, 5 patients with total gastrectomy, and 20 normal subjects. The mean basal level of plasma GIP in totally gastrectomized patients was significantly higher than in normal subjects, while in duodenal ulcer patients the value was not different from that of controls. Plasma GIP and insulin responses to oral glucose loading were significantly higher than normal in both groups. The degree of exaggerated plasma GIP and insulin secretions was more prominent and earlier in totally gastrectomized patients than in duodenal ulcer patients, and was positively correlated with the blood glucose increase during glucose ingestion. On the other hand, no significant change in GIP secretion during insulin-induced hypoglycaemia was observed in normal subjects, duodenal ulcer patients, or patients with selective proximal vagotomy. These findings indicate that the exaggerated GIP response to oral glucose in duodenal ulcer patients may be due not to increased vagal tone, but to more rapid incoming load. We found also that the hypersecretion of GIP induced by glucose ingestion in patients with duodenal ulcer and total gastrectomy may be responsible for the hyperfunction of the enteroinsular axis in these patients.