Glucose Suppresses ATP-Inhibited K-Channels in Pancreatic β-Cells

  • D. L. Cook
  • C. N. Hales
  • L. S. Satin
Part of the Advances in Experimental Medicine and Biology book series (AEMB, volume 211)


Glucose-induced insulin release involves a cascade of events in the pancreatic β-cell: the metabolism of glucose enhances the net uptake of calcium by the cell, mobilizes calcium from stores within the cell and thus triggers the exocytosis of insulin15. Calcium uptake occurs when glucose depolarizes the β-cell membrane to trigger periodic bursts of calcium action potentials2,3,10,13. The mechanisms which couple glucose metabolism to the depolarization have eluded workers since the late 1960’s. Depolarization is accompanied by increased cell input impedance, decreased dependence of membrane potential on external K+ 2, and decreased efflux of 42K+ and 86Rb+8, all of which depend on glucose metabolism9,12. These findings have suggested the existence of membrane K-channels which are open in low glucose and are closed by a process linked to glucose metabolism. As possibilities, it has been suggested that Ca-activated K-channels are closed by a glucose-induced fall of intracellular free Ca2+ 2, or that K-channels are closed by metabolic proton production and intracellular acidification14.


Pancreatic Islet Cell Periodic Burst Block Channel Activity Calcium Action Potentials2 Physiologic Membrane Potential 
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Copyright information

© Plenum Press, New York 1986

Authors and Affiliations

  • D. L. Cook
    • 1
    • 2
  • C. N. Hales
    • 3
  • L. S. Satin
    • 1
    • 2
  1. 1.Departments of Physiology and BiophysicsUniversity of WashingtonSeattleUSA
  2. 2.Department of MedicineThe Seattle VA Medical CenterSeattleUSA
  3. 3.Department of Clinical BiochemistryCambridge UniversityCambridgeEngland

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