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Glucose homeostasis is regulated by pancreatic beta-cell cilia via endosomal EphA-processing.
Nat. Commun. 10:5686 (2019)
Diabetes mellitus affects one in eleven adults worldwide. Most suffer from Type 2 Diabetes which features elevated blood glucose levels and an inability to adequately secrete or respond to insulin. Insulin producing beta-cells have primary cilia which are implicated in the regulation of glucose metabolism, insulin signaling and secretion. To better understand how beta-cell cilia affect glucose handling, we ablate cilia from mature beta-cells by deleting key cilia component Ift88. Here we report that glucose homeostasis and insulin secretion deteriorate over 12 weeks post-induction. Cilia/basal body components are required to suppress spontaneous auto-activation of EphA3 and hyper-phosphorylation of EphA receptors inhibits insulin secretion. In beta-cells, loss of cilia/basal body function leads to polarity defects and epithelial-to-mesenchymal transition. Defective insulin secretion from IFT88-depleted human islets and elevated pEPHA3 in islets from diabetic donors both point to a role for cilia/basal body proteins in human glucose homeostasis.
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Publication type
Article: Journal article
Document type
Scientific Article
Keywords
Bardet-biedl-syndrome; Insulin-secretion; Disruption; Receptor; Gtpase; Islets; Mouse; Mass; Endocytosis; Proteins
ISSN (print) / ISBN
2041-1723
e-ISSN
2041-1723
Journal
Nature Communications
Quellenangaben
Volume: 10,
Issue: 1,
Article Number: 5686
Publisher
Nature Publishing Group
Publishing Place
London
Non-patent literature
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Reviewing status
Peer reviewed