Novel Players in Pancreatic Islet Signaling
From Membrane Receptors to Nuclear Channels
- 1Institute of Bioengineering, Miguel Hernandez University, Alicante, Spain
- 2Department of Surgery, National University of Singapore, Singapore
- 3Department of Bioengineering, University of Washington, Seattle, Washington
- 4Division of Molecular Medicine, Department of Anesthesiology, David Geffen School of Medicine at UCLA, Los Angeles, California
- Address correspondence and reprint requests to Dr. Bernat Soria, Institute of Bioengineering, Miguel Hernandez University, San Juan Campus, Carretera Alicante-Valencia Km 87, 03550 Alicante, Spain. E-mail: bernat.soria{at}umh.es
Abstract
Glucose and other nutrients regulate many aspects of pancreatic islet physiology. This includes not only insulin release, but also insulin synthesis and storage and other aspects of β-cell biology, including cell proliferation, apoptosis, differentiation, and gene expression. This implies that in addition to the well-described signals for insulin release, other intracellular signaling mechanisms are needed. Here we describe the role of global and local Ca2+ signals in insulin release, the regulation of these signals by new membrane receptors, and the generation of nuclear Ca2+ signals involved in gene expression. An integrated view of these pathways should improve the present description of the β-cell biology and provide new targets for novel drugs.
- [Ca2+]i, intracellular Ca2+ concentration
- DP, diadenosine polyphosphate
- ER, estrogen receptor
- KATP channel; ATP-dependent K+ channel
- PKG, protein kinase G
- RRP, readily releasable pool
- VOC channel, voltage-operated Ca2+ channel
Footnotes
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This article is based on a presentation at a symposium. The symposium and the publication of this article were made possible by an unrestricted educational grant from Les Laboratoires Servier.
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- Accepted May 30, 2003.
- Received March 12, 2003.
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