The study on gastrin release with insulin-induced hypoglycemia

Abstract

We studied the mechanism of gastrin release with insulin-induced hypoglycemia by 7 series of experiments using dogs;(1) normal group, (2) medical vagotomied (M. V.) group, (3) phenoxybenzamine (POB) group, (4) 6-hydroxydopamine (6-OHDA) group, (5) truncal vagotomied (T. V.) group, (6) splanchinectomied (S. P.) group, and (7) truncal vagotomied and splanchinectomied (T. V.+S. P.) group. Each group was composed of 5 dogs.
We measured serum histamine, serum setotonin, serum norepinephrine, and serum gastrin before and after the intravenous injection of regular insulin every ten minutes for one hour. Serum histamine increased in the normal group and the M.V. group. Serum serotonin changed little in all groups. Serum norepinephrine increased in the normal group, the M. V. group, and the T. V. group, while it decreased in the sympathectomied groups except at the first ten minutes of the POB group. Serum gastrin increased in all groups except the T. V.+S. P. group. It increased remarkably in the normal group and the M. V. group, but there was not much increase in sympathectomied group.
Thus, I conclude that the mechanism of gastrin release with insulin-induced hypoglycemia is much more affected by the route of posterior hypothalamopituitoadrenal axis than by the anterior hypothalamovagal route. The increase of serum cathecolamine, histamine, and gastrin after the injection of insulin suggests that the final mediator for gastrin release is histamine.