Abstract
The serum gastrin response to insulin hypoglycemia has been assessed in patients with duodenal ulcer both before and after truncal vagotomy. Insulin hypoglycemia produces a significant rise in serum gastrin in the unoperated patient with duodenal ulcer, a smaller but significant rise after incomplete vagotomy, and no increase in gastrin after complete vagotomy. These results indicate that serum gastrin, as measured by radioimmunoassay, depends on intact vagal fibers for its release by insulin hypoglycemia.
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