Serum Gastric Inhibitory Polypeptide (GIP) in Duodenal Ulcer Disease: Relationship to Glucose Tolerance, Insulin, and Gastrin Release

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Abstract
Serum immunoreactive gastric inhibitory polypeptide (IR-GIP), gastrin (IRG) and insulin (IRI) were estimated in 41 normal weight patients with duodenal ulcer (DU) and 25 age-matched controls in response to a high caloric liquid test meal. Of 41 DU patients, 28 had a hyperglycemic glucose reponse during the test meal and 15 had a pathological oral glucose tolerance test. Fasting and food-stimulated IR-GIP and IRG levels were significantly elevated in the DU patients. Serum IRI also increased to significantly higher levels in DU patients after the test meal. The degree of the greater hormone response was dependent on the glucose increase after the test meal in the case of insulin and GIP, but not in the case of gastrin. A faster glucose absorption (possibly due to rapid initial gastric emptying or increased intestinal motility) is responsible for the high an short-lasting glucose peak and the increased GIP and insulin secretion. The GIP response could be causally related to the insulin response. Hyposecretion of GIP is ruled out as a possible factor in the pathogenesis of gastric acid hypersecretion of DU patients.