AJP - Endo Cosmo Bio: Excellent Endocrine ELISAs
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
 QUICK SEARCH:   [advanced]


     


Am J Physiol Endocrinol Metab 251: E86-E91, 1986;
0193-1849/86 $5.00
This Article
Right arrow Full Text (PDF)
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
Citing Articles
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Bihoreau, M. T.
Right arrow Articles by Picon, L.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Bihoreau, M. T.
Right arrow Articles by Picon, L.

AJP - Endocrinology and Metabolism, Vol 251, Issue 1 86-E91, Copyright © 1986 by American Physiological Society


ARTICLES

Effect of gestational hyperglycemia on insulin secretion in vivo and in vitro by fetal rat pancreas

M. T. Bihoreau, A. Ktorza, A. Kervran and L. Picon

The effects of gestational hyperglycemia on B-cell function were studied in near-term fetuses from unrestrained pregnant rats made slightly or highly hyperglycemic using continuous glucose infusion during the last week of pregnancy. Pancreatic and plasma insulin and insulin secretion in vitro were studied in the fetuses. Compared with controls, slightly hyperglycemic fetuses showed increased pancreatic and plasma insulin concentrations and similar insulin release in response to glucose in vitro. In highly hyperglycemic fetuses, pancreatic and plasma insulin concentrations were unchanged compared with controls, and insulin release in vitro was insensitive to glucose and to the mixture glucose plus theophylline. These results confirm that glucose is able to stimulate insulin secretion in normal or slightly hyperglycemic fetuses and suggest that severe hyperglycemia per se, without association of other metabolic disorders or toxic injuries, profoundly alters the stimulus-secretion coupling of the fetal rat B-cell.





HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Visit Other APS Journals Online