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

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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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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: Ravier, Magalie A.
Wollheim, Claes B.
Henquin, Jean-Claude
Meda, Paolo
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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Loss of Connexin36 Channels Alters β-Cell Coupling, Islet Synchronization of Glucose-Induced Ca2+ and Insulin Oscillations, and Basal Insulin Release

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