Mobilization of Different Pools of Glucose-Incorporated Calcium in Pancreatic β-Cells after Muscarinic Receptor Activation

Abstract

The introduction of new techniques and access to clonal lines of insulin-secreting cells have resulted in a re-evaluation of how glucose affects Ca²⁺ movements in the pancreatic β-cells. Contrary to previous views that calcium mobilization from intracellular stores is an important factor in glucose stimulated insulin release^30,35 and that the sugar inhibits the extrusion of Ca²⁺ from the β-cells^20,35, it was demonstrated that glucose has the opposite effects^14–16. The action of glucose on the cytoplasmic Ca²⁺ regulating insulin release can consequently be regarded as reflecting the balance between increased entry of Ca²⁺ into the β-cells and the enhanced removal of the ion from the cytoplasm following intracellular trapping and stimulated outward transport. Although each of these three important movements of Ca²⁺ are stimulated, individual differences exist with regard to the latency of the effects and their sensitivity to the glucose stimulus. Moreover, with the prolongation of the exposure to glucose the promotion of the intracellular buffering of Ca²⁺ becomes less pronounced due to a limited capacity for sequestration.