Mobilization of Different Pools of Glucose-Incorporated Calcium in Pancreatic β-Cells after Muscarinic Receptor Activation
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 release30,35 and that the sugar inhibits the extrusion of Ca2+ from the β-cells20,35, it was demonstrated that glucose has the opposite effects14–16. 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.
KeywordsPancreatic Islet Muscarinic Receptor Insulin Release Glucose Stimulation Inositol Trisphosphate
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