A Potassium Channel Modulated by Glucose Metabolism in Rat Pancreatic β-Cells

  • F. M. Ashcroft
  • D. E. Harrison
  • S. J. H. Ashcroft
Part of the Advances in Experimental Medicine and Biology book series (AEMB, volume 211)


It is well established that glucose-stimulated insulin release from the pancreatic β-cell is associated with the initiation of electrical activity (see recent review by Henquin & Meissner10). Microelectrode recordings have shown that in the absence of glucose the β-cell is electrically silent. Increasing plasma glucose depolarises the membrane by an amount that is dependent on the glucose concentration and electrical activity is initiated when this depolarisation exceeds a threshold level. There is considerable evidence that the initial slow depolarisation induced by glucose results from a decrease in the resting potassium permeability of the membrane5,8,14 as a consequence of glucose metabolism9).


Single Channel Current Channel Open Probability Increase Plasma Glucose Potassium Permeability Open State Probability 


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Copyright information

© Plenum Press, New York 1986

Authors and Affiliations

  • F. M. Ashcroft
    • 1
    • 2
  • D. E. Harrison
    • 1
    • 2
  • S. J. H. Ashcroft
    • 1
    • 2
  1. 1.University Laboratory of PhysiologyOxfordEngland
  2. 2.Nuffield Department of Clinical BiochemistryJohn Radcliffe HospitalHeadington, OxfordEngland

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