Abstract
An increase in gastric acid secretion after resection or bypass of the small bowel has been described by several authors in man and dogs1,2,3. Furthermore, a high incidence of peptic ulcer disease has been observed in patients with small bowel resection4,5. The mechanism which induces gastric hypersecretion after exclusion of large parts of the small bowel from food passage is still poorly understood. Several authors have described hypergastrinemia after small bowel exclusion or bypass, which may be caused by either a decrease in catabolism or a diminished release of inhibitors from the small intestine6,7,8. One of the physiologically important inhibitors of gastric acid secretion may be the gastric inhibitory polypeptide (GIP) which is released from the duodenum and jejunum after food intake and shows besides its insulinotropic effect a strong inhibition of stimulated acid secretion in dogs9.
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