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 calorie liquid test meal. 28 out of 41 DU patients had a hyperglycaemic glucose response 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. It is concluded: firstly, that a faster glucose absorption (possibly due to rapid initial gastric emptying or increased intestinal motility) is responsible for the high and short-lasting glucose peak and the increased GIP and insulin secretion; secondly, that the GIP response could well be causally related to the insulin response; thirdly, that hyposcretion of GIP is ruled out as a possible factor in the pathogenesis of gastric acid hypersecretion of duodenal ulcer patients.

No abstract

The trophic effect of truncal vagotomy was studied in rats. Three months after vagotomy and pyloroplasty pancreatic weight was significantly increased by 40% (p < 0.001). Gastric stasis and consecutive distension of the stomach was observed in the majority of vagotomized animals despite pyloroplasty; the trophic effect of vagotomy on the pancreas was most pronounced in animals with severe stomach distension. Basal gastrin levels were increased after truncal vagotomy but did not correlate to gastric stasis and to the hypertrophy and hyperplasia of the exocrine pancreas. Basal pancreatic polypeptide hexapeptide levels were not altered after vagotomy. Morphometric studies on the endocrine pancreatic tissue showed that the relative volume density decreased due to the increase in exocrine tissue. However, the total islet cell mass remained constant. It is concluded that chronic truncal vagotomy has a trophic effect on the exocrine but not on the endocrine pancreas; additional factors besides gastrin seem to be responsible for this.

Different types of vagotomy have been widely used in the treatment of peptic ulcer disease. A close relationship between the vagus nerve and the release or action of gastrointestinal hormones is necessary for the optimal activation of the gastrointestinal tract. The serum concentrations of the antral hormone gastrin are elevated after all types of vagotomy. The postvagotomy hypergastrinemia is due to the change in pH in the antral lumen or the gastric motility changes, both of which may lead to a proliferation of G cells. The reduction in pancreatic secretion after vagotomy is not due to changes in intestinal hormone release, but may be caused by the interruption of a postulated enteropancreatic reflex. Postprandial GIP release and serum insulin levels are not affected by vagotomy, but basal GIP levels are increased after vagotomy. Postprandial pancreatic polypeptide release is nearly abolished by vagotomy, but seems to normalize in the later postoperative course. These findings may be important for the interpretation of pathophysiologic changes after vagotomy.

No abstract