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This Article Full Text Full Text (PDF) All Versions of this Article: JOE-08-0261v1 199/1/1    most recent Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Similar articles in Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Hodgkin, M N Articles by Squires, P E Search for Related Content PubMed PubMed Citation Articles by Hodgkin, M N Articles by Squires, P E

Department of Biological Sciences, University of Warwick, Coventry CV4 7AL, UK¹ Department of Infection, Immunity and Inflammation, Leicester School of Medicine, University of Leicester, PO Box 138, Leicester LE1 7RH, UK

(Correspondence should be addressed to P E Squires; Email: p.e.squires{at}warwick.ac.uk)

In the 15 years since the identification and characterisation of the extracellular calcium-sensing receptor (CaR), it has become increasingly apparent that this cationic binding receptor is found in many tissues, not associated with the control of plasma calcium. One of these tissues is the pancreatic islet where insulin secretion provides the basis of energy regulation. It seems inherently unlikely that the islet responds to alterations in systemic calcium and a more plausible and intriguing possibility is that the CaR mediates cell-to-cell communication through local increases in the concentration of extracellular Ca²⁺, co-released with insulin. This short article explores this possibility and suggests that this novel mechanism of cell communication, along with direct coupling via gap junctions and other local paracrine regulators helps explain why the glucose responsiveness of the intact islet is greater than the sum of the composite parts in isolation.