HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text Full Text (PDF) Purchase Article View Shopping Cart Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Permissions Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Westerlund, J. Articles by Bergsten, P. Search for Related Content PubMed PubMed Citation Articles by Westerlund, J. Articles by Bergsten, P. Social Bookmarking                What's this?

Glucose Metabolism and Pulsatile Insulin Release From Isolated Islets

Department of Medical Cell Biology, Uppsala University, Uppsala, Sweden

The effects of metabolic inhibition on insulin release and the cytoplasmic Ca²⁺ concentration ([Ca²⁺]_i) were studied in individually perifused pancreatic islets from ob/ob mice. The modest basal secretion in the presence of 3 mmol/l glucose was pulsatile with a frequency of 0.2/min, although [Ca²⁺]_i was stable at 100 nmol/l. Introduction of 11 mmol/l glucose resulted in large amplitude oscillations of [Ca²⁺]_i and almost 20-fold stimulation of average secretion manifested as increased amplitude of the insulin pulses without change in frequency. Inhibition of glycolysis with iodoacetamide or mitochondrial metabolism with dinitrophenol or antimycin A reduced glucose-stimulated secretion back to basal levels with maintained pulsatility. The [Ca²⁺]_i responses to the metabolic inhibitors were more complex, but in general there was an initial peak and eventually sustained elevation without oscillations. When introduced in the presence of 3 mmol/l glucose, the metabolic inhibitors tended to increase the amplitude of the insulin pulses, although the simultaneous elevation in [Ca²⁺]_i occurred without oscillations. The data indicate that pulsatile secretion is regulated by factors other than [Ca²⁺]_i under basal conditions and after metabolic inhibition. Although pulsatile secretion can be driven by oscillations in metabolism when [Ca²⁺]_i is stable, it was not possible from the present data to determine whether insulin pulses have a glycolytic or mitochondrial origin.

CiteULike

Del.icio.us

Digg

Reddit

Technorati

This article has been cited by other articles:

				D. S. Luciani, S. Misler, and K. S. Polonsky Ca2+ controls slow NAD(P)H oscillations in glucose-stimulated mouse pancreatic islets J. Physiol., April 15, 2006; 572(2): 379 - 392. [Abstract] [Full Text] [PDF]

				S. Gopel, Q. Zhang, L. Eliasson, X.-S. Ma, J. Galvanovskis, T. Kanno, A. Salehi, and P. Rorsman Capacitance measurements of exocytosis in mouse pancreatic {alpha}-, {beta}- and {delta}-cells within intact islets of Langerhans J. Physiol., May 1, 2004; 556(3): 711 - 726. [Abstract] [Full Text] [PDF]

				S. Srivastava and H. J. Goren Insulin Constitutively Secreted by {beta}-Cells Is Necessary for Glucose-Stimulated Insulin Secretion Diabetes, August 1, 2003; 52(8): 2049 - 2056. [Abstract] [Full Text] [PDF]

				R. A. Ritzel, J. D. Veldhuis, and P. C. Butler Glucose Stimulates Pulsatile Insulin Secretion from Human Pancreatic Islets by Increasing Secretory Burst Mass: Dose-Response Relationships J. Clin. Endocrinol. Metab., February 1, 2003; 88(2): 742 - 747. [Abstract] [Full Text] [PDF]