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EGF receptor in pancreatic beta-cell mass regulation.

Authors
  • Miettinen, Päivi
  • Ormio, Päivi
  • Hakonen, Elina
  • Banerjee, Meenal
  • Otonkoski, Timo
Type
Published Article
Journal
Biochemical Society transactions
Publication Date
Jun 01, 2008
Volume
36
Issue
Pt 3
Pages
280–285
Identifiers
DOI: 10.1042/BST0360280
PMID: 18481942
Source
Medline
License
Unknown

Abstract

Pancreatic islet development is impaired in mice lacking EGFRs (epidermal growth factor receptors). Even partial tissue-specific attenuation of EGFR signalling in the islets leads to markedly reduced beta-cell proliferation and development of diabetes during the first weeks after birth. Out of the many EGFR ligands, betacellulin has been specifically associated with positive effects on beta-cell growth, through both increased proliferation and neogenesis. EGFR action is also necessary for the beta-cell mitogenic activity of the gut hormone GLP-1 (glucagon-like peptide 1). Finally, in vitro models demonstrate a central role for EGFR in transdifferentiation of pancreatic acinar and ductal cells into endocrine islet cells. EGFR thus plays an essential role in beta-cell mass regulation, but its mechanisms of action remain poorly understood.

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