Regulation of Insulin Secretion in Islets of Langerhans by Ca2+Channels

Regulation of Insulin Secretion in Islets of Langerhans by Ca2+Channels Insulin secretion from β-cells of the pancreatic islets of Langerhans is triggered by Ca2+ influx through voltage-dependent Ca2+ channels. Electrophysiological and molecular studies indicate that β-cells express several subtypes of these channels. This review discusses their roles in regulating insulin secretion, focusing on recent studies using β-cells, exogenous expression systems, and Ca2+ channel knockout mice. These investigations reveal that L-type Ca2+ channels in the β-cell physically interact with the secretory apparatus by binding to synaptic proteins on the plasma membrane and insulin granule. As a result, Ca2+ influx through L-type channels efficiently and rapidly stimulates release of a pool of insulin granules in close contact with the channels. Thus, L-type Ca2+ channel activity is preferentially coupled to exocytosis in the β-cell, and plays a critical role in regulating the dynamics of insulin secretion. Non-L-type channels carry a significant portion of the total voltage-dependent Ca2+ current in β-cells and cell lines from some species, but nevertheless account for only a small fraction of insulin secretion. These channels may regulate exocytosis indirectly by affecting membrane potential or second messenger signaling pathways. Finally, voltage-independent Ca2+ entry pathways and their potential roles in β-cell function are discussed. The emerging picture is that Ca2+ channels regulate insulin secretion at multiple sites in the stimulus-secretion coupling pathway, with the specific role of each channel determined by its biophysical and structural properties. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png The Journal of Membrane Biology Springer Journals

Regulation of Insulin Secretion in Islets of Langerhans by Ca2+Channels

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Publisher
Springer-Verlag
Copyright
Copyright © 2004 by Springer Science+Business Media, Inc.
Subject
Life Sciences; Human Physiology; Biochemistry, general
ISSN
0022-2631
eISSN
1432-1424
D.O.I.
10.1007/s00232-004-0692-9
Publisher site
See Article on Publisher Site

Abstract

Insulin secretion from β-cells of the pancreatic islets of Langerhans is triggered by Ca2+ influx through voltage-dependent Ca2+ channels. Electrophysiological and molecular studies indicate that β-cells express several subtypes of these channels. This review discusses their roles in regulating insulin secretion, focusing on recent studies using β-cells, exogenous expression systems, and Ca2+ channel knockout mice. These investigations reveal that L-type Ca2+ channels in the β-cell physically interact with the secretory apparatus by binding to synaptic proteins on the plasma membrane and insulin granule. As a result, Ca2+ influx through L-type channels efficiently and rapidly stimulates release of a pool of insulin granules in close contact with the channels. Thus, L-type Ca2+ channel activity is preferentially coupled to exocytosis in the β-cell, and plays a critical role in regulating the dynamics of insulin secretion. Non-L-type channels carry a significant portion of the total voltage-dependent Ca2+ current in β-cells and cell lines from some species, but nevertheless account for only a small fraction of insulin secretion. These channels may regulate exocytosis indirectly by affecting membrane potential or second messenger signaling pathways. Finally, voltage-independent Ca2+ entry pathways and their potential roles in β-cell function are discussed. The emerging picture is that Ca2+ channels regulate insulin secretion at multiple sites in the stimulus-secretion coupling pathway, with the specific role of each channel determined by its biophysical and structural properties.

Journal

The Journal of Membrane BiologySpringer Journals

Published: Jan 1, 2004

References

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