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Islets. 2010 Mar-Apr;2(2):59-64. doi: 10.4161/isl.2.2.11171.

Electrical activity in pancreatic islet cells: The VRAC hypothesis.

Author information

1
University of Manchester, UK. Len.Best@cmft.nhs.uk

Abstract

A major aspect of stimulation of β-cell function by glucose is the induction of electrical activity. The ionic events that underlie β-cell electrical activity are understood in some detail. At sub-stimulatory glucose concentrations, the β-cell is electrically 'silent'. Increasing the glucose concentration to stimulatory levels results in a gradual depolarisation of the membrane potential to a threshold potential where 'spikes' or action potentials are generated. These action potentials represent the gating of voltage-sensitive Ca²(+) channels, leading to Ca²(+) entry into the cell, thus triggering the release of insulin. The stimulatory actions of glucose on the β-cell depend on the metabolism of the hexose. A major question concerns the molecular mechanism(s) whereby β-cell plasma membrane potential is regulated by changes in glucose metabolism in the cell. This article provides a brief summary of the evidence suggesting that, in addition to metabolically-regulated K(ATP) channels, β-cells are equipped with a volume-regulated anion channel that is activated by glucose concentrations within the range effective in modulating electrical activity and insulin release.

PMID:
21099297
DOI:
10.4161/isl.2.2.11171
[Indexed for MEDLINE]

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