| Experimental models of beta-cell regeneration. | |
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MedLine Citation:
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PMID: 18481943 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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The control of glucose metabolism by pancreatic endocrine cells throughout life relies on a tight regulation of the mass of insulin-producing beta-cells. How this homoeostasis is achieved is not well understood. Over the last few years, experimental rodent models with altered beta-cell mass, and, more recently, new transgenic approaches designed to tackle this problem, have provided abundant information. Processes such as beta-cell proliferation and apoptosis, or even beta-cell differentiation from poorly characterized progenitor cells, whether immature or differentiated, appear to be implicated. A complex picture is thus emerging in which the nature of the pancreatic lesion appears to determine the kind of regenerative response. The environment formed by acinar and ductal cells, and also by vascular and neuronal structures, which surround islets and penetrate into their beta-cell core, might play crucial roles so far unsuspected, which should be explored in the near future. |
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Authors:
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Claire Bonal; Isabelle Avril; Pedro L Herrera |
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Publication Detail:
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Type: Journal Article; Review |
Journal Detail:
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Title: Biochemical Society transactions Volume: 36 ISSN: 0300-5127 ISO Abbreviation: Biochem. Soc. Trans. Publication Date: 2008 Jun |
Date Detail:
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Created Date: 2008-05-16 Completed Date: 2008-11-03 Revised Date: - |
Medline Journal Info:
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Nlm Unique ID: 7506897 Medline TA: Biochem Soc Trans Country: England |
Other Details:
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Languages: eng Pagination: 286-9 Citation Subset: IM |
Affiliation:
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Department of Genetic Medicine and Development, University of Geneva Medical School, 1 rue Michel-Servet, CH-1211 Geneva 4, Switzerland. |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Animals Humans Insulin-Secreting Cells / pathology* Models, Biological* Regeneration* |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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