Mechanisms of coordination of Ca2+ signals in pancreatic islet cells

Federico Bertuzzi, Alberto M. Davalli, Rita Nano, Carlo Socci, Franca Codazzi, Riccardo Fesce, Valerio Di Carlo, Guido Pozza, Fabio Grohovaz

Research output: Contribution to journalArticlepeer-review


Within pancreatic islet cells, rhythmic changes in the cytosolic Ca2+ concentration have been reported to occur in response to stimulatory glucose concentrations and to be synchronous with pulsatile release of insulin. We explored the possible mechanisms responsible for Ca2+ signal propagation within islet cells, with particular regard to gap junction communication, the pathway widely credited with being responsible for coordination of the secretory activity. Using fura-2 imaging, we found that multiple mechanisms control Ca2+ signaling in pancreatic islet cells. Gap junction blockade by 18 α-glycyrrhetinic acid greatly restricted the propagation of Ca2+ waves induced by mechanical stimulation of cells but affected neither Ca2+ signals nor insulin secretion elicited by glucose elevation. The source of Ca2+ elevation was also different under the two experimental conditions, the first being sustained by release from inner stores and the second by nifedipine-sensitive Ca2+ influx. Furthermore, glucose-induced Ca2+ waves were able to propagate across cell-free clefts, indicating that diffusible factors can control Ca2+ signal coordination. Our results provide evidence that multiple mechanisms of Ca2+ signaling operate in β-cells and that gap junctions are not required for intercellular Ca2+ wave propagation or insulin secretion in response to glucose.

Original languageEnglish
Pages (from-to)1971-1978
Number of pages8
Issue number10
Publication statusPublished - Oct 1999

ASJC Scopus subject areas

  • Internal Medicine
  • Endocrinology, Diabetes and Metabolism


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