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Open Access Green as soon as Postprint is submitted to ZB.
EphA-Ephrin-A-Mediated ß cell communication regulates insulin secretion from pancreatic islets.
Cell 129, 359-370 (2007)
In vertebrates, ß cells are aggregated in the form of pancreatic islets. Within these islets, communication between ß cells inhibits basal insulin secretion and enhances glucose-stimulated insulin secretion, thus contributing to glucose homeostasis during fasting and feeding. In the search for the underlying molecular mechanism, we have discovered that ß cells communicate via ephrin-As and EphAs. We provide evidence that ephrin-A5 is required for glucose-stimulated insulin secretion. We further show that EphA-ephrin-A-mediated ß cell communication is bidirectional: EphA forward signaling inhibits insulin secretion, whereas ephrin-A reverse signaling stimulates insulin secretion. EphA forward signaling is downregulated in response to glucose, which indicates that, under basal conditions, ß cells use EphA forward signaling to suppress insulin secretion and that, under stimulatory conditions, they shift to ephrin-A reverse signaling to enhance insulin secretion. Thus, we explain how ß cell communication in pancreatic islets conversely affects basal and glucose-stimulated insulin secretion to improve glucose homeostasis.
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Publication type
Article: Journal article
Document type
Scientific Article
Keywords
cellbio; humidisease
Language
english
Publication Year
2007
HGF-reported in Year
0
ISSN (print) / ISBN
0092-8674
e-ISSN
1097-4172
Journal
Cell
Quellenangaben
Volume: 129,
Pages: 359-370
Publisher
Cell Press
Publishing Place
Cambridge, Mass.
Reviewing status
Peer reviewed
Institute(s)
Institute of Developmental Genetics (IDG)
POF-Topic(s)
30204 - Cell Programming and Repair
Research field(s)
Genetics and Epidemiology
PSP Element(s)
G-500500-001
PubMed ID
17448994
Erfassungsdatum
2007-04-20