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This Article Accepted manuscript (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 PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Squires, P. Articles by Hills, C. Search for Related Content PubMed PubMed Citation Articles by Squires, P. Articles by Hills, C.

P Squires, Biologcal Sciences, The University of Warwick, Coventry, CV4 7AL, United Kingdom
M Hodgkin, Biological Science, University of Warwick, Coventry, United Kingdom
C Hills, Infection, Immunity and Inflammation, University of Leicester, Leicester, United Kingdom

Correspondence: Paul Squires, Email: p.e.squires{at}warwick.ac.uk

Abstract

In the 15years since the identification and characterisation of the extracellular calcium-sensing receptor (CaR), it has become increasing apparent that this cationic binding receptor is found on 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 commentary explores this possibility and suggests that this novel mechanism of cell communication, along with direct coupling via gap-junction 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.