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Cited by 360Pancreatic function and diabetesConnexins and lens biologyDiabetes and associated disorders

The DOI matches its Crossref record; 53 of the 53 references it cites were found in a registry or an index.

Loss of Connexin36 Channels Alters β-Cell Coupling, Islet Synchronization of Glucose-Induced Ca2+ and Insulin Oscillations, and Basal Insulin Release

Ravier, Magalie A., Güldenagel, Martin, Charollais, Anne, Gjinovci, Asllan, Caille, Dorothée, Söhl, Goran, Wollheim, Claes B., Willecke, Klaus, Henquin, Jean-Claude, Meda, Paolo·2005·Diabetes
DOI 10.2337/diabetes.54.6.1798
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Abstract

Normal insulin secretion requires the coordinated functioning of β-cells within pancreatic islets. This coordination depends on a communications network that involves the interaction of β-cells with extracellular signals and neighboring cells. In particular, adjacent β-cells are coupled via channels made of connexin36 (Cx36). To assess the function of this protein, we investigated islets of transgenic mice in which the Cx36 gene was disrupted by homologous recombination. We observed that compared with wild-type and heterozygous littermates that expressed Cx36 and behaved as nontransgenic controls, mice homozygous for the Cx36 deletion (Cx36−/−) featured β-cells devoid of gap junctions and failing to exchange microinjected Lucifer yellow. During glucose stimulation, islets of Cx36−/− mice did not display the regular oscillations of intracellular calcium concentrations ([Ca2+]i) seen in controls due to the loss of cell-to-cell synchronization of [Ca2+]i changes. The same islets did not release insulin in a pulsatile fashion, even though the overall output of the hormone in response to glucose stimulation was normal. However, under nonstimulatory conditions, islets lacking Cx36 showed increased basal release of insulin. These data show that Cx36-dependent signaling is essential for the proper functioning of β-cells, particularly for the pulsatility of [Ca2+]i and insulin secretion during glucose stimulation.

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Crossref · 10.2337/diabetes.54.6.1798

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Metadata

Authors
Ravier, M. A., Güldenagel, M., Charollais, A., Gjinovci, A., Caille, D., Söhl, G., Wollheim, C. B., Willecke, K., Henquin, J.-C., & Meda, P.
Affiliations
  • UCLouvain (BE)
  • Institute of Genetics, University of Bonn, Bonn, Germany
  • University of Geneva (CH)
  • Department of Cell Physiology and Metabolism, Geneva University Medical Center, Geneva, Switzerland
  • University of Bonn (DE)
ORCID
Venue
Diabetes
Publisher
American Diabetes Association
Published
2005-06-01
Volume
54
Issue
6
Pages
1798-1807
ISSN
  • 0012-1797 (ISSN-L)
  • 1939-327X
DOI
10.2337/diabetes.54.6.1798
OpenAlex
W2108896758
Cited by
360
References
52
Citations by year
2026: 11 · 2025: 8 · 2024: 12 · 2023: 19 · 2022: 20 · 2021: 28 · 2020: 19 · 2019: 12 · 2018: 10 · 2017: 19 · 2016: 18 · 2015: 19 · 2014: 26 · 2013: 24 · 2012: 25
FWCI
16.74
Type
journal article
Language
en
Open access
closed
Locations
  • Diabetes (publishedVersion)
  • PubMed (publishedVersion)
  • DIAL (Catholic University of Leuven) (submittedVersion)
  • UCL Discovery (University College London) (submittedVersion)
Funders
  • Schweizerischer Nationalfonds zur Förderung der Wissenschaftlichen Forschung
  • National Institute of Diabetes and Digestive and Kidney Diseases (R01-DK63443, R01DK063443)
Topics
  • Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Pancreatic function and diabetes
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Connexins and lens biology
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Diabetes and associated disorders
Keywords
connexin 36, gap junctions, pancreatic islets, insulin secretion, calcium oscillations, insulin oscillations, glucose-stimulated insulin secretion
MeSH terms
Gap Junction delta-2 Protein, Animals, Calcium, Female, Glucose, Heterozygote, Homozygote, Insulin, Islets of Langerhans, Male, Connexins, Mice, Knockout, Mice

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