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 Bergsten, P. Search for Related Content PubMed PubMed Citation Articles by Bergsten, P. Social Bookmarking                What's this?

Role of Oscillations in Membrane Potential, Cytoplasmic Ca²⁺, and Metabolism for Plasma Insulin Oscillations

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

A model for the relationship between ionic and metabolic oscillations and plasma insulin oscillations is presented. It is argued that the pancreatic ß-cell in vivo displays two intrinsic frequencies that are important for the regulation of plasma insulin oscillations. The rapid oscillatory activity (2–7 oscillations [osc] per minute), which is evident in both ionic and metabolic events, causes the required elevation in cytoplasmic Ca²⁺ concentration ([Ca²⁺]_i) for the exocytosis of insulin granules. This activity is important for regulation of the amplitude of plasma insulin oscillations. The frequency of the rapid oscillatory ionic activities is regulated by glucose and allows the ß-cell to respond in an analogous way, with gradual changes in [Ca²⁺]_i and insulin release in response to the alterations in glucose concentration. The slower oscillatory activity (0.2–0.4 osc/min), which is evident in the metabolism of the ß-cell, has a frequency corresponding to the frequency observed in plasma insulin oscillations. The frequency is not affected by changes in the glucose concentration. This activity is suggested to generate energy in a pulsatile fashion, which sets the frequency of the plasma insulin oscillations. It is proposed that the slow oscillations in [Ca²⁺]_i observed in vitro are a manifestation of the metabolic oscillations and do not represent an in vivo phenomenon.

CiteULike

Del.icio.us

Digg

Reddit

Technorati

This article has been cited by other articles:

				M. Zhang, B. Fendler, B. Peercy, P. Goel, R. Bertram, A. Sherman, and L. Satin Long Lasting Synchronization of Calcium Oscillations by Cholinergic Stimulation in Isolated Pancreatic Islets Biophys. J., November 15, 2008; 95(10): 4676 - 4688. [Abstract] [Full Text] [PDF]

				L. S. Farhy, Z. Du, Q. Zeng, P. P. Veldhuis, M. L. Johnson, K. L. Brayman, and A. L. McCall Amplification of pulsatile glucagon counterregulation by switch-off of {alpha}-cell-suppressing signals in streptozotocin-treated rats Am J Physiol Endocrinol Metab, September 1, 2008; 295(3): E575 - E585. [Abstract] [Full Text] [PDF]

				W. Gartner, G. Vila, T. Daneva, A. Nabokikh, F. Koc-Saral, A. Ilhan, O. Majdic, A. Luger, and L. Wagner New functional aspects of the neuroendocrine marker secretagogin based on the characterization of its rat homolog Am J Physiol Endocrinol Metab, July 1, 2007; 293(1): E347 - E354. [Abstract] [Full Text] [PDF]

				L. E. Fridlyand, L. Ma, and L. H. Philipson Adenine nucleotide regulation in pancreatic {beta}-cells: modeling of ATP/ADP-Ca2+ interactions Am J Physiol Endocrinol Metab, November 1, 2005; 289(5): E839 - E848. [Abstract] [Full Text] [PDF]

				C. S. Nunemaker, R. A. DeFazio, and S. M. Moenter Calcium Current Subtypes in GnRH Neurons Biol Reprod, December 1, 2003; 69(6): 1914 - 1922. [Abstract] [Full Text] [PDF]

				C. J. Barker, I. B. Leibiger, B. Leibiger, and P.-O. Berggren Phosphorylated inositol compounds in beta -cell stimulus-response coupling Am J Physiol Endocrinol Metab, December 1, 2002; 283(6): E1113 - E1122. [Abstract] [Full Text] [PDF]