Calcium signaling in pancreatic β-cells in health and in Type 2 diabetes

Cell Calcium. 2014 Nov;56(5):340-61. doi: 10.1016/j.ceca.2014.09.001. Epub 2014 Sep 8.


Changes in cytosolic free Ca(2+) concentration ([Ca(2+)]c) play a crucial role in the control of insulin secretion from the electrically excitable pancreatic β-cell. Secretion is controlled by the finely tuned balance between Ca(2+) influx (mainly through voltage-dependent Ca(2+) channels, but also through voltage-independent Ca(2+) channels like store-operated channels) and efflux pathways. Changes in [Ca(2+)]c directly affect [Ca(2+)] in various organelles including the endoplasmic reticulum (ER), mitochondria, the Golgi apparatus, secretory granules and lysosomes, as imaged using recombinant targeted probes. Because most of these organelles have specific Ca(2+) influx and efflux pathways, they mutually influence free [Ca(2+)] in the others. In this article, we review the mechanisms of control of [Ca(2+)] in various compartments and particularly the cytosol, the endoplasmic reticulum ([Ca(2+)]ER), acidic stores and mitochondrial matrix ([Ca(2+)]mito), focusing chiefly on the most important physiological stimulus of β-cells, glucose. We also briefly review some alterations of β-cell Ca(2+) homeostasis in Type 2 diabetes.

Keywords: Calcium signaling; Diabetes; β-Cells.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Calcium / metabolism*
  • Calcium Signaling / genetics*
  • Diabetes Mellitus, Type 2 / genetics*
  • Diabetes Mellitus, Type 2 / metabolism
  • Diabetes Mellitus, Type 2 / pathology
  • Endoplasmic Reticulum / genetics
  • Endoplasmic Reticulum / pathology
  • Glucose / metabolism
  • Humans
  • Insulin / metabolism
  • Insulin-Secreting Cells / metabolism
  • Insulin-Secreting Cells / pathology
  • Islets of Langerhans


  • Insulin
  • Glucose
  • Calcium