Abstract
AbstractHypoglycemic release of gastrin has been supposed solely to be due to vagal release. In this report the atropine resistance of the gastrin response to insulin was examined. 9 normal subjects were studied twice. 0.2 IU of insulin/kg i.v. was injected in each study, but in one atropine (30 μg/kg i.m.) was injected prior to insulin. Serum gastrin concentrations were measured by radioimmunoassay. Blood glucose concentrations did not differ in the two studies. Atropine almost abolished gastric output of acid. Gastrin concentrations rose after insulin and slightly more after atropinization. In four of the subjects a second late gastrin increase was observed after atropine. It is concluded that in man a major part of the hypoglycemic release of gastrin is independent on a cholinergic mechanism.
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