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Cited by 1,113Pancreatic function and diabetesIon channel regulation and functionIon Transport and Channel Regulation

Glucose induces closure of single potassium channels in isolated rat pancreatic β-cells

Ashcroft, Frances M., Harrison, Donna E., Ashcroft, Stephen J. H.·1984·Nature
DOI 10.1038/312446a0
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Abstract

The major physiological stimulus for the secretion of insulin from the pancreatic beta-cell is an increase in the plasma glucose concentration. It is well established that glucose-stimulated insulin secretion is associated with the appearance of electrical activity in the beta-cell; glucose concentrations above the threshold level for insulin release produce a slow membrane depolarization followed by either oscillatory bursts of action potentials (5-15 mM glucose) or continuous spiking (greater than 16 mM glucose). Tracer flux studies and microelectrode measurements using intact islets of Langerhans have indicated that the initial depolarization induced by glucose is caused by a decrease in the resting membrane permeability to potassium. Evidence also suggests that the electrical, ionic and secretory responses to glucose are mediated by the metabolism of the sugar within the beta-cell. By using cell-attached membrane patches from isolated rat pancreatic beta-cells, we have now identified a potassium channel (G-channel) that is active at the resting potential and is inhibited by glucose. Closure of this channel requires glucose metabolism. This is the first report of a potassium channel whose activity is modulated by glucose, and which may couple metabolic and ionic events involved in the secretion of insulin.

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  • Glucose metabolism closes the KATP channel, thereby depolarizing the β-cell and initiating β-cell electrical activity, Ca2+ influx and insulin secretion.

    “Glucose metabolism closes the KATP channel, thereby depolarizing the β-cell and initiating β-cell electrical activity, Ca2+ influx and insulin secretion (27, 573).”

    From Pancreatic β-Cell Electrical Activity and Insulin Secretion: Of Mice and Men (2018) · cites this paper as [27]

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Authors
Ashcroft, F. M., Harrison, D. E., & Ashcroft, S. J. H.
Affiliations
University of Oxford (GB)
ORCID
Ashcroft, Frances M.
Venue
Nature
Publisher
Springer Science and Business Media LLC
Published
1984-11
Volume
312
Issue
5993
Pages
446-448
ISSN
  • 0028-0836 (ISSN-L)
  • 1476-4687
DOI
10.1038/312446a0
OpenAlex
W1994924615
Cited by
1,113
References
0
Citations by year
2026: 12 · 2025: 16 · 2024: 23 · 2023: 23 · 2022: 29 · 2021: 35 · 2020: 10 · 2019: 22 · 2018: 22 · 2017: 24 · 2016: 22 · 2015: 27 · 2014: 36 · 2013: 29 · 2012: 34
FWCI
40.02
Type
journal article
Language
en
Open access
closed
Licence
www.springer.com/tdm (tdm)
Locations
  • Nature (publishedVersion)
  • PubMed (publishedVersion)
Topics
  • Health Sciences › Medicine › Surgery › Pancreatic function and diabetes
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Ion channel regulation and function
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Ion Transport and Channel Regulation
Keywords
glucose, potassium channels, pancreatic beta cells, insulin secretion, glucose-stimulated insulin secretion, glucose metabolism, membrane depolarization, resting membrane potential
MeSH terms
Action Potentials, Animals, Glucose, Ion Channels, Islets of Langerhans, Kinetics, Membrane Potentials, Potassium, Rats, In Vitro Techniques

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