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Cited by 78Pancreatic function and diabetesIon channel regulation and functionCardiac electrophysiology and arrhythmias

Ion channels and regulation of insulin secretion in human β-cells: a computational systems analysis

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Fridlyand, Leonid E., Jacobson, David A., Philipson, L.H.·2013·Islets
DOI 10.4161/isl.24166PMC PMC3662377
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Abstract

In mammals an increase in glucose leads to block of ATP dependent potassium channels in pancreatic β cells leading to membrane depolarization. This leads to the repetitive firing of action potentials that increases calcium influx and triggers insulin granule exocytosis. Several important differences between species in this process suggest that a dedicated human-oriented approach is advantageous as extrapolating from rodent data may be misleading in several respects. We examined depolarization-induced spike activity in pancreatic human islet-attached β-cells employing whole-cell patch-clamp methods. We also reviewed the literature concerning regulation of insulin secretion by channel activity and constructed a data-based computer model of human β cell function. The model couples the Hodgkin-Huxley-type ionic equations to the equations describing intracellular Ca²⁺ homeostasis and insulin release. On the basis of this model we employed computational simulations to better understand the behavior of action potentials, calcium handling and insulin secretion in human β cells under a wide range of experimental conditions. This computational system approach provides a framework to analyze the mechanisms of human β cell insulin secretion.

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  • Meglitinides increase insulin release by inhibiting ATP-sensitive potassium channels, depolarizing β-cells, and opening calcium channels, which let calcium into the cells.

    “They increase the release of insulin by inhibiting ATP-sensitive potassium channels, which depolarize β-cells, and opening calcium channels, which let calcium in.”

    From A critical review on diabetes mellitus type 1 and type 2 management approaches: from lifestyle modification to current and novel targets and therapeutic agents. (2024) · cites this paper as [62]

    The Introduction (page unavailable) describes KATP-channel closure leading to β-cell depolarization, voltage-dependent calcium entry, and insulin secretion. The KATP channels section (page unavailable) likewise reports increased calcium and insulin secretion when KATP conductance falls. Our copy does not identify meglitinides as the drugs acting through this mechanism; its named KATP-blocking drug example is tolbutamide. (LLM, conf=0.86)

    Experimental — accuracy not yet measured

  • Production of insulin is stimulated by elevated calcium levels in the cells.

    “Production of insulin is stimulated by elevated calcium in the cells levels (61, 62).”

    From A critical review on diabetes mellitus type 1 and type 2 management approaches: from lifestyle modification to current and novel targets and therapeutic agents. (2024) · cites this paper as [62]

    The Introduction (page unavailable) says a rise in cytosolic Ca2+ helps control insulin secretion, and the section on Ca2+ and insulin exocytosis describes calcium-triggered release of insulin granules. These passages support stimulated insulin release, but not the claim that elevated calcium stimulates insulin production or synthesis. (LLM, conf=0.86)

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Cited by

Sorted by citations

Authors
Fridlyand, L. E., Jacobson, D. A., & Philipson, L. H.
Affiliations
  • University of Chicago (US)
  • Vanderbilt University (US)
Corresponding author
Fridlyand, Leonid E.
ORCID
Venue
Islets
Publisher
Informa UK Limited
Published
2013-01
Volume
5
Issue
1
Pages
1-15
ISSN
  • 1938-2014 (ISSN-L)
  • 1938-2022
DOI
10.4161/isl.24166
PMC
PMC3662377
OpenAlex
W2072984035
Cited by
78
References
10
Citations by year
2026: 1 · 2025: 6 · 2024: 5 · 2023: 3 · 2022: 3 · 2021: 10 · 2020: 8 · 2019: 6 · 2018: 13 · 2017: 9 · 2016: 4 · 2015: 3 · 2014: 7
FWCI
0.83
Type
journal article
Language
en
Open access
Licence
cc-by-nc
Locations
  • Islets (publishedVersion, cc-by-nc)
  • Europe PMC (PubMed Central) (publishedVersion, cc-by-nc)
  • PubMed Central (publishedVersion, cc-by-nc)
  • PubMed (publishedVersion)
Funders
  • W. M. Keck Foundation
  • National Institute of Diabetes and Digestive and Kidney Diseases (DK-063493, R01DK048494, R01DK063493, DK-48494, P60DK020595)
Topics
  • Health Sciences › Medicine › Surgery › Pancreatic function and diabetes
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Ion channel regulation and function
  • Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiac electrophysiology and arrhythmias
Keywords
insulin secretion, pancreatic beta cells, ion channels, ATP-sensitive potassium channels, membrane depolarization, action potential, calcium handling, insulin granule exocytosis, human islets, Hodgkin-Huxley model, glucose regulation
MeSH terms
Insulin Secretion, Animals, Computer Simulation, Humans, Insulin, Ion Channels, Models, Biological, Species Specificity, Calcium Signaling, Insulin-Secreting Cells, Secretory Pathway

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