Action potentials and insulin secretion: new insights into the role of Kv channels
Article first published online: 4 OCT 2007
DOI: 10.1111/j.1463-1326.2007.00784.x
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How to Cite
Jacobson, D. A. and Philipson, L. H. (2007), Action potentials and insulin secretion: new insights into the role of Kv channels. Diabetes, Obesity and Metabolism, 9: 89–98. doi: 10.1111/j.1463-1326.2007.00784.x
Publication History
- Issue published online: 4 OCT 2007
- Article first published online: 4 OCT 2007
- Received 1 March 2007; accepted 6 June 2007
- Abstract
- Article
- References
- Cited By
Keywords:
- delayed rectifier;
- electrical activity;
- hannatoxin;
- islet;
- Kv2.1;
- potassium channel;
- stromatoxin
Coordinated electrical activity allows pancreatic β-cells to respond to secretagogues with calcium entry followed by insulin secretion. Metabolism of glucose affects multiple membrane proteins including ion channels, transporters and pumps that collaborate in a cascade of electrical activity resulting in insulin release. Glucose induces β-cell depolarization resulting in the firing of action potentials (APs), which are the primary electrical signal of the β-cell. They are shaped by orchestrated activation of ion channels. Here we give an overview of the voltage-gated potassium (Kv) channels of the β-cell, which are responsible in part for the falling phase of the AP, and how their regulation affects insulin secretion. β cells contain several Kv channels allowing dynamic integration of multiple signals on repolarization of glucose-stimulated APs. Recent studies on Kv channel regulation by cAMP and arachidonic acid and on the Kv2.1 null mouse have greatly increased our understanding of β-cell excitation–secretion coupling.

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