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. The Journal of Membrane Biology Springer Journals

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

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Copyright © 2004 by Springer Science+Business Media, Inc.
Life Sciences; Human Physiology; Biochemistry, general
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