AJP - Endocrinology and Metabolism, Vol 256, Issue 3 E431-E438, Copyright © 1989 by American Physiological Society
Response of gut glucagon-like immunoreactivity to hypoglycemia in dogs
A. Ohneda, I. Sasaki, H. Naito, M. Toda, M. Ohneda and F. Koizumi
First Department of Surgery, Tohoku University School of Medicine, Sendai, Japan.
Previous studies demonstrated that insulin-induced hypoglycemia enhances
glicentin secretion in piglets and prompted us to investigate the response
of glucagon-like immunoreactivity (GLI) to hypoglycemia in dogs. Insulin
hypoglycemia did not induce any rise of plasma total immunoreactive
glucagon (IRG) measured by nonspecific antiserum to glucagon in normal or
pancreatectomized dogs under anesthesia. In contrast, insulin-induced
hypoglycemia clearly increased plasma total IRG in both normal and
pancreatectomized dogs in a conscious state. Administration of
acetylcholine resulted in an elevation of plasma total IRG, whereas
epinephrine induced a slight increase in plasma total IRG. The infusion of
alpha- or beta-adrenergic blockers did not affect the response of plasma
total IRG to hypoglycemia, whereas atropine completely blunted the increase
in plasma total IRG during insulin hypoglycemia. Similarly atropine
abolished the rise of plasma total IRG during intravenous administration of
2-deoxy-D-glucose. It is concluded that hypoglycemia clearly enhances the
secretion of GLI from the gut in dogs and that GLI secretion during
hypoglycemia is modulated, at least in part, by the autonomic nervous
system.
