AJP - Regulatory, Integrative and Comparative Physiology, Vol 246, Issue 6 985-R993, Copyright © 1984 by American Physiological Society
Glucose responsiveness and acetylcholine sensitivity of pancreatic beta-cells after vagotomy
L. A. Campfield, F. J. Smith and R. E. Eskinazi
The chronic effects of removal of parasympathetic neural input to the
pancreas on in vitro insulin secretion were assessed. Groups of Wistar and
Long-Evans rats received total subdiaphragmatic vagotomy or sham operation.
Four to ten weeks later, after the return of food intake and body weight in
the vagotomized groups to values similar to the sham-operated groups,
pancreatic islets were isolated and statically incubated with selected
concentrations of glucose and acetylcholine. Two experimental protocols
were used. In the first experiment, insulin secretion in response to basal
(5 mM) glucose was 59 +/- 15 (SE) and 65 +/- 13% greater in islets from the
vagotomized Wistar and Long-Evans groups, respectively, than in the
corresponding sham groups. The enhancement of insulin secretion by several
doses of acetylcholine observed in islets from sham-operated groups was
totally absent in islets from both vagotomized strains. In the second
experiment, insulin secretion was determined in response to selected
glucose concentrations by using islets from Wistar rats. An upward and
leftward shift of the dose-response curve was observed in the vagotomized
group causing 5 mM to become a stimulatory glucose concentration and
increasing the stimulatory potency of 10 mM glucose. These results suggest
that interruption of vagal input to pancreatic beta-cells may induce a
compensatory increase in responsiveness to glucose and a functional
suppression of acetylcholine receptors. These data provide further support
for the hypothesis that vagal input plays a functionally important role in
the control of insulin secretion and maintenance of acetylcholine
sensitivity.
