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 Asplund, K.
Right arrow Articles by Freinkel, N.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Asplund, K.
Right arrow Articles by Freinkel, N.
Social Bookmarking
 Add to CiteULike   Add to Del.icio.us   Add to Digg   Add to Reddit   Add to Technorati  
What's this?

Diabetes, Vol 27, Issue 6 611-619, Copyright © 1978 by American Diabetes Association


ARTICLES

Phosphate metabolism and glucose-initiated efflux of phosphate ions in islets of fetal pancreas

K Asplund and N Freinkel

Elsewhere we have proposed that the rapid transient efflux of 32P orthophosphate that occurs when prelabeled pancreatic islets are exposed to nutrient secretagogues (the "phosphate flush") reflects one of the earliest steps in islet stimulus-secretion coupling. We have now shown that the "phosphate flush" is much smaller with islets from fetal rats 21 1/2 days old. This could be attributed to decreased cellular stores of radioactivity, especially inorganic orthophosphate (32P), at the onset of stimulation, which may have been due, in part, to the diminished ability of fetal islets to retain the radiophosphorus accumulated during the labeling period. Certain other differences in phosphate metabolism were also observed. With prelabeled islets from adult rats, exposure to 3.0 mg. per milliliter glucose effected acute increases in the tissue content of AT32P and GT32P. Comparable stimulation of prelabeled fetal islets with 3.0 mg. per milliliter glucose did not elicit detectable changes in the labeling of ATP or GTP. The findings indicate that selected aspects of phosphate metabolism may be immature in fetal islets and, perhaps, implicated in their obtunded secretion of insulin in response to stimulation with glucose.
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
J. Biol. Chem.Home page
L. K. Olson, W. Schroeder, R. P. Robertson, N. D. Goldberg, and T. F. Walseth
Suppression of Adenylate Kinase Catalyzed Phosphotransfer Precedes and Is Associated with Glucose-induced Insulin Secretion in Intact HIT-T15 Cells
J. Biol. Chem., July 12, 1996; 271(28): 16544 - 16552.
[Abstract] [Full Text] [PDF]




HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Diabetes Diabetes Care Clinical Diabetes Diabetes Spectrum
Copyright © 1978 by the American Diabetes Association.