ROLE OF THE SYMPATHOADRENAL SYSTEM IN EXERCISE-INDUCED INHIBITION OF INSULIN-SECRETION - EFFECTS OF ISLET TRANSPLANTATION

Citation
H. Houwing et al., ROLE OF THE SYMPATHOADRENAL SYSTEM IN EXERCISE-INDUCED INHIBITION OF INSULIN-SECRETION - EFFECTS OF ISLET TRANSPLANTATION, Diabetes, 44(5), 1995, pp. 565-571
Citations number
45
Categorie Soggetti
Endocrynology & Metabolism","Medicine, General & Internal
Journal title
ISSN journal
00121797
Volume
44
Issue
5
Year of publication
1995
Pages
565 - 571
Database
ISI
SICI code
0012-1797(1995)44:5<565:ROTSSI>2.0.ZU;2-Q
Abstract
The present study was designed to investigate the mechanism leading to inhibition of insulin release during exercise. To investigate the inf luence of circulating epinephrine and norepinephrine, these catecholam ines were infused intravenously in resting islet-transplanted and cont rol rats. The role of neural influences on insulin release was investi gated by a swimming: exercise study in islet-transplanted and control rats, before and after adrenodemedullation., Streptozotocin-induced di abetic Albino Oxford rats received 5 mu l islet tissue into the portal vein, resulting in return of normal basal glucose and insulin levels. Transplanted and control animals were provided with two permanent hea rt catheters to sample blood and to give infusions. Infusion of epinep hrine and norepinephrine did not result in inhibition of plasma insuli n levels. Blood glucose levels, as well as nonesterified fatty acids a nd insulin levels in plasma, were similar in both groups. After the in fusion study, the animals were subjected to strenuous swimming. During exercise, plasma insulin levels decreased not only in controls, but a lso in the islet-transplanted group, Blood glucose and plasma catechol amine responses were identical in both groups. After adrenodemedullati on, epinephrine was not detectable and the exercise-induced decrease o f insulin was not affected. These results indicate that circulating ep inephrine and norepinephrine in physiological concentrations do not ca use inhibit;ion of insulin secretion. Since the exercise-induced inhib ition of insulin secretion is still present in rats with islet grafts, it seems reasonable to suggest that sympathetic neural influences are responsible for the inhibition of insulin release during exercise and that transplanted islets are sympathetically reinnervated.