Standard Article

Electrophysiology of the β Cell and Mechanisms of Inhibition of Insulin Release

Handbook of Physiology, The Endocrine System, The Endocrine Pancreas and Regulation of Metabolism

  1. Mark J. Dunne1,
  2. Carina Ämmälä2,
  3. Susanne G. Straub3,
  4. Geoffrey W. G. Sharp3

Published Online: 1 JAN 2011

DOI: 10.1002/cphy.cp070204

Comprehensive Physiology

Comprehensive Physiology

How to Cite

Dunne, M. J., Ämmälä, C., Straub, S. G. and Sharp, G. W. G. 2011. Electrophysiology of the β Cell and Mechanisms of Inhibition of Insulin Release. Comprehensive Physiology. 79–123.

Author Information

  1. 1

    Department of Biomedical Science, University of Sheffield Western Bank, Sheffield, United Kingdom

  2. 2

    Department of Molecular Endocrinology, Glaxo Wellcome, Research Triangle Park, North Carolina

  3. 3

    Department of Pharmacology, College of Veterinary Medicine, Cornell University, Ithaca, New York

Publication History

  1. Published Online: 1 JAN 2011

Abstract

The sections in this article are:

  • 1
    Ion Channels in Insulin-Secreting Cells
    • 1.1
      Adenosine Triphosphate–Sensitive Potassium Channels
    • 1.2
      Extracellular Control of Adenosine Triphosphate-Sensitive Potassium Channel Function
    • 1.3
      Therapeutic Manipulation by Modulators of Adenosine Triphosphate-Sensitive Potassium Channels
    • 1.4
      Architecture of the β-cell Adenosine Triphosphate-Sensitive Potassium Channel
    • 1.5
      Calcium-Selective Ion Channels
    • 1.6
      Voltage-Gated Sodium Channels
    • 1.7
      Voltage-Gated Potassium Channels
    • 1.8
      Voltage-Independent Potassium Channels
    • 1.9
      Nonselective Cation Channels
    • 1.10
      Anion-Selective Channels
  • 2
    Ionic Defects of β-Cell Function
    • 2.1
      Persistent Hyperinsulinemic Hypoglycemia of Infancy
    • 2.2
      Altered Ionic Control of β Cells and Hypersecretion of Insulin
    • 2.3
      Correlation of Gene Defects in the Adenosine Triphosphate-Sensitive Potassium Channel with Persistent Hyperinsulinemic Hypoglycemia of Infancy
    • 2.4
      Clinical Therapy for Persistent Hyperinsulinemic Hypoglycemia of Infancy
    • 2.5
      Implications for Diabetes Mellitus
  • 3
    Stimulus-Secretion Coupling Mechanisms Other Than Depolarization
  • 4
    Novel Methods for the Measurement of Insulin Secretion
    • 4.1
      Capacitance
    • 4.2
      Amperometry and Voltametry
    • 4.3
      Calcium and Exocytosis
    • 4.4
      Cyclic Adenosine Monophosphate and Exocytosis
    • 4.5
      Effects of Phospholipases and Protein Kinases C and A
    • 4.6
      Sulfonylureas and Exocytosis
    • 4.7
      G Proteins and Exocytosis
    • 4.8
      Other Modulators of Exocytosis
    • 4.9
      Modeling Calcium-, Cyclic, and Adenosine Monophosphate–, and Guanosine Triphosphate–Dependent Exocytosis
  • 5
    Molecular Mechanisms of Exocytosis in the β Cell
  • 6
    Receptor-Mediated Inhibition of Insulin Release: Early and Late Effects
    • 6.1
      Involvement of G Proteins
    • 6.2
      Receptor–G Protein Interactions
  • 7
    Inhibitory Mechanisms
    • 7.1
      Adenosine Triphosphate–Sensitive Potassium Channel Activation and Membrane Repolarization
    • 7.2
      Calcium Channel Inhibition
    • 7.3
      Inhibition of Adenylate Cyclase
    • 7.4
      Inhibition at a Distal Site
  • 8
    G Protein–Target Interactions
    • 8.1
      Adenosine Triphosphate–Sensitive Potassium Channel
    • 8.2
      L-Type Calcium Channels
    • 8.3
      Adenylate Cyclase
    • 8.4
      Distal Inhibitory Site
  • 9
    Other Possible Mechanisms
    • 9.1
      Inhibition of Glucose Metabolism
    • 9.2
      Inhibition of Fatty Acid Metabolism
    • 9.3
      Stimulation of Calcium–Adenosine Triphosphatase Activity
    • 9.4
      Cyclic Guanosine Monophosphate
    • 9.5
      Cytoskeleton
  • 10
    Summary of Inhibitory Mechanisms