Islet‐cell‐to‐cell communication as basis for normal insulin secretion

No abstract is available for this paper.

• Publication year

  2007

• Venue

  Diabetes, obesity and metabolism

• Publication date

  2007-10-04

• Fields of study

  Biology, Medicine

• Identifiers
  DOI 10.1111/j.1463-1326.2007.00780.xPMID 17919186
• External record

  Open on Semantic Scholar

• Source metadata

  Semantic Scholar, PubMed

• No claims are published for this paper.

• No concepts are published for this paper.

• Faculty Opinions recommendation of EphA-Ephrin-A-mediated beta cell communication regulates insulin secretion from pancreatic islets.

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  2006cited by this paper
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  2006cited by this paper
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  2005cited by this paper
• The connexins, Part III.

  2005cited by this paper
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  2005cited by this paper
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  2005cited by this paper
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  2005cited by this paper
• Replacement by a lacZ reporter gene assigns mouse connexin36, 45 and 43 to distinct cell types in pancreatic islets.

  2004cited by this paper
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  2004cited by this paper
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  2003cited by this paper
• Lentivirus-mediated transduction of connexin cDNAs shows level- and isoform-specific alterations in insulin secretion of primary pancreaticβ -cells

  2003cited by this paper
• Critical Role of the Transcriptional Repressor Neuron-restrictive Silencer Factor in the Specific Control of Connexin36 in Insulin-producing Cell Lines*

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  2002cited by this paper
• Genome-Wide Search for Type 2 Diabetes in Japanese Affected Sib-Pairs Confirms Susceptibility Genes on 3 q , 15 q , and 20 q and Identifies Two New Candidate Loci on 7 p and 11 p

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• Genome-wide search for type 2 diabetes in Japanese affected sib-pairs confirms susceptibility genes on 3q, 15q, and 20q and identifies two new candidate Loci on 7p and 11p.

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• beta-cell-specific deletion of the Igf1 receptor leads to hyperinsulinemia and glucose intolerance but does not alter beta-cell mass.

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• Overexpression of dominant-negative mutant hepatocyte nuclear fctor-1 alpha in pancreatic beta-cells causes abnormal islet architecture with decreased expression of E-cadherin, reduced beta-cell proliferation, and diabetes.

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• Overexpression of Dominant-Negative Mutant Hepatocyte Nuclear Factor-1α in Pancreatic β-Cells Causes Abnormal Islet Architecture With Decreased Expression of E-Cadherin, Reduced β-cell Proliferation, and Diabetes

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• Measurements of cytoplasmic Ca2+ in islet cell clusters show that glucose rapidly recruits beta-cells and gradually increases the individual cell response.

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• Emerging issues of connexin channels: biophysics fills the gap

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  2001cited by this paper
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  2000cited by this paper
• Gap junction function

  2000cited by this paper
• Cx36 preferentially connects beta-cells within pancreatic islets.

  2000cited by this paper
• Association of connexin36 with zonula occludens-1 in HeLa cells, βTC-3 cells, pancreas, and adrenal gland

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• Loci on chromosomes 2 (NIDDM1) and 15 interact to increase susceptibility to diabetes in Mexican Americans

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• Adequate connexin-mediated coupling is required for proper insulin production

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• Actively synthesizing beta-cells secrete preferentially after glucose stimulation.

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• Repeated glucose stimulation reveals distinct and lasting secretion patterns of individual rat pancreatic B cells.

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• Ion channels of glucose-responsive and -unresponsive beta-cells.

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• Actively Synthesizing β-Cells Secrete Preferentially after Glucose Stimulation

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• Ion Channels of Glucose-Responsive and -Unresponsive β-cells

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  1989cited by this paper
• Impaired pulsatile secretion of insulin in relatives of patients with non-insulin-dependent diabetes.

  1988cited by this paper
• The gap junction: a channel for multiple functions?

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• Stimulation of insulin secretion reveals heterogeneity of pancreatic B cells in vivo.

  1987cited by this paper
• Heterogeneity and contact-dependent regulation of hormone secretion by individual B cells.

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  1976cited by this paper
• A morphological basis for intercellular communication between alpha- and beta-cells in the endocrine pancreas.

  1975cited by this paper
• Structural coupling between pancreatic islet cells

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