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 Hill, R. S.
Right arrow Articles by Boyd, A. E.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Hill, R. S.
Right arrow Articles by Boyd, A. E.
Social Bookmarking
Add to CiteULike   Add to Del.icio.us   Add to Digg   Add to Reddit   Add to Technorati  
What's this?

Diabetes, Vol 36, Issue 4 440-446, Copyright © 1987 by American Diabetes Association

ARTICLES

Increase in cAMP levels in beta-cell line potentiates insulin secretion without altering cytosolic free-calcium concentration

RS Hill, JM Oberwetter and AE Boyd

With an SV40-transformed hamster beta-cell line (HIT cells) as a model system, we tested the hypothesis that a rise in cAMP levels potentiates insulin release by an effect on the cytosolic free-Ca2+ concentration ([Ca2+]i). Intracellular cAMP levels were measured by radioimmunoassay, and [Ca2+]i was monitored with the fluorescent Ca2+ indicator quin 2. Insulin secretion was followed in static incubations or perifusion of the cells. In perifusion, both high glucose and depolarization of the beta-cell with 40 mM K+ trigger a monophasic pattern of insulin release without altering the HIT cell cAMP content. Addition of either the phosphodiesterase inhibitor isobutylmethylxanthine (IBMX) or the adenylate cyclase activator forskolin dramatically increased the cellular cAMP content, potentiated the burst phase of insulin release, and coupled the immediate phase of insulin secretion to a sustained secretory response. However, increases in cellular cAMP content were not associated with a change in [Ca2+]i. Thus, the potentiation of insulin secretion by a rise in cAMP in the HIT cell is not mediated by a release of stored Ca2+. Either a glucose-generated signal or a rise in [Ca2+]i triggered by high K+ can synergize with a rise in cAMP to couple the burst or immediate release of insulin evoked by either secretagogue to the sustained release of insulin.
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. Physiol.Home page
H. Hatakeyama, T. Kishimoto, T. Nemoto, H. Kasai, and N. Takahashi
Rapid glucose sensing by protein kinase A for insulin exocytosis in mouse pancreatic islets
J. Physiol., January 15, 2006; 570(2): 271 - 282.
[Abstract] [Full Text] [PDF]

Home page
 Am. J. Physiol. Endocrinol. Metab.Home page
J. An, G. Zhao, L. M. Churgay, J. J. Osborne, J. E. Hale, G. W. Becker, G. Gold, L. E. Stramm, and Y. Shi
Threonine phosphorylations induced by RX-871024 and insulin secretagogues in beta TC6-F7 cells
Am J Physiol Endocrinol Metab, November 1, 1999; 277(5): E862 - E869.
[Abstract] [Full Text] [PDF]


HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Diabetes Diabetes Care Clinical Diabetes Diabetes Spectrum
Copyright © 1987 by the American Diabetes Association.