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Islet Studies

β-Cell Secretory Products Activate α-Cell ATP-Dependent Potassium Channels to Inhibit Glucagon Release

  1. Isobel Franklin1,
  2. Jesper Gromada2,
  3. Asllan Gjinovci1,
  4. Sten Theander1 and
  5. Claes B. Wollheim1
  1. 1Department of Cell Physiology and Metabolism, University Medical Centre, Geneva, Switzerland
  2. 2Lilly Research Laboratories, Hamburg, Germany
  1. Address correspondencereprint requests to Dr. Claes B. Wollheim, Department of Cell PhysiologyMetabolism, University Medical Centre, 1211 Geneva 4, Switzerland. E-mail: claes.wollheim{at}medicine.unige.ch
Diabetes 2005 Jun; 54(6): 1808-1815. https://doi.org/10.2337/diabetes.54.6.1808
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Article Information

vol. 54 no. 6 1808-1815
DOI 
https://doi.org/10.2337/diabetes.54.6.1808
PubMed 
15919803

Published By 
American Diabetes Association
Print ISSN 
0012-1797
Online ISSN 
1939-327X
History 
  • March 16, 2005
  • January 26, 2005
  • Published in print May 25, 2005.

Copyright & Usage 
DIABETES

Author Information

  1. Isobel Franklin1,
  2. Jesper Gromada2,
  3. Asllan Gjinovci1,
  4. Sten Theander1 and
  5. Claes B. Wollheim1
  1. 1Department of Cell Physiology and Metabolism, University Medical Centre, Geneva, Switzerland
  2. 2Lilly Research Laboratories, Hamburg, Germany
  1. Address correspondencereprint requests to Dr. Claes B. Wollheim, Department of Cell PhysiologyMetabolism, University Medical Centre, 1211 Geneva 4, Switzerland. E-mail: claes.wollheim{at}medicine.unige.ch
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β-Cell Secretory Products Activate α-Cell ATP-Dependent Potassium Channels to Inhibit Glucagon Release
Isobel Franklin, Jesper Gromada, Asllan Gjinovci, Sten Theander, Claes B. Wollheim
Diabetes Jun 2005, 54 (6) 1808-1815; DOI: 10.2337/diabetes.54.6.1808

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β-Cell Secretory Products Activate α-Cell ATP-Dependent Potassium Channels to Inhibit Glucagon Release
Isobel Franklin, Jesper Gromada, Asllan Gjinovci, Sten Theander, Claes B. Wollheim
Diabetes Jun 2005, 54 (6) 1808-1815; DOI: 10.2337/diabetes.54.6.1808
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  • Glucagon Resistance and Decreased Susceptibility to Diabetes in a Model of Chronic Hyperglucagonemia
  • Acyl-Ghrelin Influences Pancreatic β-Cell Function by Interference with KATP Channels
  • Pancreatic β-Cell–Specific Deletion of VPS41 Causes Diabetes Due to Defects in Insulin Secretion
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