AJP - Endo Fuel your research with LabChart
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH
 QUICK SEARCH:   [advanced]


     


Am J Physiol Endocrinol Metab (April 24, 2007). doi:10.1152/ajpendo.00647.2006
This Article
Right arrow Full Text (PDF)
Right arrow All Versions of this Article:
293/1/E396    most recent
00647.2006v1
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 HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Bertuzzi, A.
Right arrow Articles by Mingrone, G.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Bertuzzi, A.
Right arrow Articles by Mingrone, G.
Submitted on November 27, 2006
Accepted on April 16, 2007

INSULIN GRANULE TRAFFICKING IN B-CELLS: MATHEMATICAL MODEL OF GLUCOSE-INDUCED INSULIN SECRETION

Alessandro Bertuzzi1, Serenella Salinari2, and Geltrude Mingrone3*

1 Institute of Systems Analysis and Computer Science, CNR, Rome, Italy
2 Department of Systems Analysis and Informatics, University of Rome ``La Sapienza'', Rome, Italy
3 Istituto di Clinica Medica, Università Cattolica S. Cuore, Rome, Italy

* To whom correspondence should be addressed. E-mail: gmingrone{at}rm.unicatt.it.

A mathematical model that represents the dynamics of intracellular insulin granules in {beta}-cells is proposed. Granule translocation and exocytosis are controlled by signals assumed to be essentially related to ATP/ADP ratio and cytosolic Ca2+ concentration. The model provides an interpretation of the roles of the triggering and amplifying pathways of glucose-stimulated insulin secretion. Values of most of the model parameters were inferred from available experimental data. The numerical simulations represent a variety of experimental conditions, such as the stimulation by high K+ and by different time courses of extracellular glucose, and the predicted responses agree with published experimental data. Model capacity to represent data measured in a hyperglycemic clamp was also tested. Model parameter changes that may reflect alterations of {beta}-cell function present in type 2 diabetes are investigated, and the action of pharmacological agents that bind to sulfonylurea receptors is simulated.




This article has been cited by other articles:


Home page
Biophys. JHome page
Y.-d. Chen, S. Wang, and A. Sherman
Identifying the Targets of the Amplifying Pathway for Insulin Secretion in Pancreatic {beta}-Cells by Kinetic Modeling of Granule Exocytosis
Biophys. J., September 1, 2008; 95(5): 2226 - 2241.
[Abstract] [Full Text] [PDF]




HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH
Visit Other APS Journals Online
Copyright © 2007 by the American Physiological Society.