This Article Full Text Full Text (PDF) All Versions of this Article: biophysj.106.087296v1 91/6/2082    most recent Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Nunemaker, C. S. Articles by Satin, L. S. Search for Related Content PubMed PubMed Citation Articles by Nunemaker, C. S. Articles by Satin, L. S.

Glucose Modulates [Ca²⁺]_i Oscillations in Pancreatic Islets via Ionic and Glycolytic Mechanisms

Craig S. Nunemaker ^*, Richard Bertram , Arthur Sherman , Krasimira Tsaneva-Atanasova , Camille R. Daniel   and Leslie S. Satin ^*

^* Department of Pharmacology and Toxicology, Virginia Commonwealth University, Richmond, Virginia; Department of Mathematics and Programs in Neuroscience and Molecular Biophysics, Florida State University, Tallahassee, Florida; Laboratory of Biological Modeling, National Institutes of Health, Bethesda, Maryland; and Virginia Tech, Department of Mathematics, Blacksburg, Virginia

Correspondence: Address reprint requests to Dr. Leslie S. Satin, Tel.: 804-828-7823; E-mail: lsatin{at}hsc.vcu.edu.

Pancreatic islets of Langerhans display complex intracellular calcium changes in response to glucose that include fast (seconds), slow (5 min), and mixed fast/slow oscillations; the slow and mixed oscillations are likely responsible for the pulses of plasma insulin observed in vivo. To better understand the mechanisms underlying these diverse patterns, we systematically analyzed the effects of glucose on period, amplitude, and plateau fraction (the fraction of time spent in the active phase) of the various regimes of calcium oscillations. We found that in both fast and slow islets, increasing glucose had limited effects on amplitude and period, but increased plateau fraction. In some islets, however, glucose caused a major shift in the amplitude and period of oscillations, which we attribute to a conversion between ionic and glycolytic modes (i.e., regime change). Raising glucose increased the plateau fraction equally in fast, slow, and regime-changing islets. A mathematical model of the pancreatic islet consisting of an ionic subsystem interacting with a slower metabolic oscillatory subsystem can account for these complex islet calcium oscillations by modifying the relative contributions of oscillatory metabolism and oscillatory ionic mechanisms to electrical activity, with coupling occurring via K_ATP channels.

This article has been cited by other articles:

				G. G. Holz, E. Heart, and C. A. Leech Synchronizing Ca2+ and cAMP oscillations in pancreatic {beta}-cells: a role for glucose metabolism and GLP-1 receptors?Focus on "Regulation of cAMP dynamics by Ca2+ and G protein-coupled receptors in the pancreatic {beta}-cell: a computational approach" Am J Physiol Cell Physiol, January 1, 2008; 294(1): C4 - C6. [Full Text] [PDF]

				R. Bertram, L. S. Satin, M. G. Pedersen, D. S. Luciani, and A. Sherman Interaction of Glycolysis and Mitochondrial Respiration in Metabolic Oscillations of Pancreatic Islets Biophys. J., March 1, 2007; 92(5): 1544 - 1555. [Abstract] [Full Text] [PDF]