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Cited by 110Pancreatic function and diabetesDiabetes Treatment and ManagementIon channel regulation and function

Multisite regulation of insulin secretion by cAMP-increasing agonists: evidence that glucagon-like peptide 1 and glucagon act via distinct receptors

Gromada, J., Ding, Wei-Guang, Barg, Sebastian, Renström, Erik, Rorsman, Patrik·1997·Pfl�gers Archiv European Journal of Physiology
DOI 10.1007/s004240050431
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Abstract

The mechanisms by which glucagon-like peptide 1(7-36)amide (GLP-1[7-36]amide) potentiates insulin secretion were investigated by measurements of whole-cell K+ and Ca2+ currents, membrane potential, the cytoplasmic Ca2+ concentration ([Ca2+]i) and exocytosis in mouse pancreatic B-cells. GLP-1(7-36)amide (10 nM) stimulated glucose-induced (10 mM) electrical activity in intact pancreatic islets. The effect was manifested as a 34% increase in the duration of the bursts of action potentials and a corresponding 28% shortening of the silent intervals. GLP-1(7-36)amide had no effect on the electrical activity at subthreshold glucose concentrations (< or = 6.5 mM). In cultured B-cells, GLP-1(7-36)amide produced a decrease of the whole-cell ATP-sensitive K+ (KATP) conductance remaining at 5 mM glucose by approximately 30%. This effect was associated with membrane depolarization and the initiation of electrical activity. GLP-1(7-36)amide produced a protein-kinase-A-(PKA-) and glucose-dependent fourfold potentiation of Ca(2+)-induced exocytosis whilst only increasing the Ca2+ current marginally. The stimulatory action of GLP-1(7-36)amide on exocytosis was mimicked by the pancreatic hormone glucagon and exendin-4, a GLP-1 receptor agonist. Whereas the stimulatory action of GLP-1(7-36)amide could be antagonized by exendin-(9-39), this peptide did not interfere with the ability of glucagon to stimulate exocytosis. We suggest that GLP-1(7-36)amide and glucagon stimulate insulin secretion by…

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  • HCN channels may therefore contribute to the reported shortening of the interburst interval observed in β-cells of mouse islets exposed to high (50 nM) concentrations of GLP-1.

    “HCN channels may therefore contribute to the reported shortening of the interburst interval observed in β-cells (211) of mouse islets exposed to high (50 nM) concentrations of GLP-1 (238).”

    From Pancreatic β-Cell Electrical Activity and Insulin Secretion: Of Mice and Men (2018) · cites this paper as [238]

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Authors
Gromada, J., Ding, W.-G., Barg, S., Renström, E., & Rorsman, P.
Affiliations
Novo Nordisk (Denmark) (DK)
ORCID
Venue
Pfl�gers Archiv European Journal of Physiology
Publisher
Springer Science and Business Media LLC
Published
1997-08-11
Volume
434
Issue
5
Pages
515-524
ISSN
  • 0031-6768 (ISSN-L)
  • 1432-2013
DOI
10.1007/s004240050431
OpenAlex
W2038182611
Cited by
110
References
2
Citations by year
2026: 2 · 2025: 3 · 2024: 2 · 2023: 2 · 2022: 2 · 2021: 5 · 2020: 6 · 2019: 1 · 2018: 2 · 2017: 3 · 2016: 4 · 2015: 2 · 2014: 9 · 2013: 3 · 2012: 4
FWCI
3.83
Type
journal article
Language
en
Open access
closed
Licence
www.springer.com/tdm (tdm)
Locations
  • Pflügers Archiv - European Journal of Physiology (publishedVersion)
  • PubMed (publishedVersion)
  • Lund University Publications (Lund University) (submittedVersion)
Topics
  • Health Sciences › Medicine › Surgery › Pancreatic function and diabetes
  • Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diabetes Treatment and Management
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Ion channel regulation and function
Keywords
insulin secretion, glucagon-like peptide-1, GLP-1(7-36)amide, glucagon, pancreatic beta cells, exocytosis, cAMP/PKA signaling, ATP-sensitive potassium channels, calcium current, electrical activity, exendin-4, exendin-9-39, receptor specificity
MeSH terms
Insulin Secretion, Cyclic AMP, Animals, Calcium, Electrophysiology, Glucagon-Like Peptides, Enzyme Activation, Exocytosis, Glucagon, Insulin, Islets of Langerhans, Mice, Inbred Strains, Peptide Fragments, Peptides, Receptors, Cell Surface, Cyclic AMP-Dependent Protein Kinases, Neurotransmitter Agents, Mice, Glucagon-Like Peptide 1, In Vitro Techniques

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