Diabetes
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
QUICK SEARCH:   [advanced]


     

This Article
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow Request Permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Loubatieres-Mariani, M. M.
Right arrow Articles by Manteghetti, M.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Loubatieres-Mariani, M. M.
Right arrow Articles by Manteghetti, M.
Social Bookmarking
Add to CiteULike   Add to Del.icio.us   Add to Digg   Add to Reddit   Add to Technorati  
What's this?

Diabetes, Vol 29, Issue 11 895-898, Copyright © 1980 by American Diabetes Association

ARTICLES

A different action of hypothermia on insulin release from the isolated, perfused rat pancreas, depending on the stimulating agent

MM Loubatieres-Mariani, J Chapa, R Puech and M Manteghetti

Two series of experiments were performed in parallel on the isolated perfused rat pancreas. The experimental conditions differed only as pertaining to temperature. In one series the organ and the perfusion liquid were maintained at 37.5 degrees C and in the other at 28 degrees C. The pancreases were perfused from the start of the experiments with a perfusion medium containing 8.3 mmol/l glucose. The effects of various stimulatory agents were studied (glucose 16.6 mmol/l, tolbutamide 0.4 mmol/l, acetylcholine 0.5 micromole/l, glucagon, 2.8 nmol/l, and L-isoprenaline 0.05 micromole/l). At 37.5 degrees C the insulin secretion induced by high glucose or tolbutamide, acetylcholine, and glucagon was biphasic and not statistically different. In all cases the hypothermia (28 degrees C) decreased insulin secretion. However, glucose-induced and tolbutamide-induced insulin secretion was more decreased than the secretion induced by acetylcholine and glucagon. The study of the secretion ratios obtained at 28 degrees C relative to 37.5 degrees C showed that the ratios for the glucose and tolbutamide groups were significantly lower than those obtained for acetylcholine and glucagon groups for both the first and the second phase. The ratios were not significantly different between glucose and tolbutamide on the one hand and acetylcholine and glucagon on the other hand. In all groups the ratios 28 degrees/37.5 degrees for the second phase were lower than those obtained during the first phase. L-isoprenaline induced only a weak increase in insulin secretion and this was not long lasting; this increase was not statistically different at both temperatures.
Add to CiteULike CiteULike   Add to Del.icio.us Del.icio.us   Add to Digg Digg   Add to Reddit Reddit   Add to Technorati Technorati    What's this?


This article has been cited by other articles:


Home page
 DiabetesHome page
K. Moens, V. Berger, J.-M. Ahn, C. Van Schravendijk, V. J. Hruby, D. Pipeleers, and F. Schuit
Assessment of the Role of Interstitial Glucagon in the Acute Glucose Secretory Responsiveness of In Situ Pancreatic {beta}-Cells
Diabetes, March 1, 2002; 51(3): 669 - 675.
[Abstract] [Full Text] [PDF]


HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Diabetes Diabetes Care Clinical Diabetes Diabetes Spectrum
Copyright © 1980 by the American Diabetes Association.