Calcium and Metabolic Oscillations in Pancreatic Islets: Who's Driving the Bus?

Watts, M., Fendler, B., Merrins, M. J., Satin, L. S., Bertram, R., Sherman, A. (April 2014) Calcium and Metabolic Oscillations in Pancreatic Islets: Who's Driving the Bus? SIAM journal on applied dynamical systems, 13 (2). pp. 683-703. ISSN 1536-0040 (Print)1536-0040

DOI: 10.1137/130920198


Pancreatic islets exhibit bursting oscillations in response to elevated blood glucose. These oscillations are accompanied by oscillations in the free cytosolic Ca2+ concentration (Cac ), which drives pulses of insulin secretion. Both islet Ca2+ and metabolism oscillate, but there is some debate about their interrelationship. Recent experimental data show that metabolic oscillations in some cases persist after the addition of diazoxide (Dz), which opens K(ATP) channels, hyperpolarizing beta-cells and preventing Ca2+ entry and Ca2+ oscillations. Further, in some islets in which metabolic oscillations were eliminated with Dz, increasing the cytosolic Ca2+ concentration by the addition of KCl could restart the metabolic oscillations. Here we address why metabolic oscillations persist in some islets but not others, and why raising Cac restarts oscillations in some islets but not others. We answer these questions using the dual oscillator model (DOM) for pancreatic islets. The DOM can reproduce the experimental data and shows that the model supports two different mechanisms for slow metabolic oscillations, one that requires calcium oscillations and one that does not.

Item Type: Paper
Subjects: organs, tissues, organelles, cell types and functions > sub-cellular tissues: types and functions > calcium channel
bioinformatics > computational biology
organs, tissues, organelles, cell types and functions > organs types and functions > metabolism
CSHL Authors:
Communities: CSHL labs > Atwal lab
Depositing User: Matt Covey
Date: April 2014
Date Deposited: 27 Feb 2015 16:15
Last Modified: 27 Feb 2015 16:15
PMCID: PMC4331037
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