GLP-1 receptor signalling promotes β-cell glucose metabolism via mTOR-dependent HIF-1α activation

Glucagon-like peptide-1 (GLP-1) promotes insulin secretion from pancreatic β-cells in a glucose dependent manner. Several pathways mediate this action by rapid, kinase phosphorylation-dependent, but gene expression-independent mechanisms. Since GLP-1-induced insulin secretion requires glucose metabo...

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Bibliographic Details
Published in:	Scientific reports Vol. 7; no. 1; pp. 2661 - 13
Main Authors:	Carlessi, Rodrigo, Chen, Younan, Rowlands, Jordan, Cruzat, Vinicius F., Keane, Kevin N., Egan, Lauren, Mamotte, Cyril, Stokes, Rebecca, Gunton, Jenny E., Bittencourt, Paulo Ivo Homem de, Newsholme, Philip
Format:	Journal Article
Language:	English
Published:	London Nature Publishing Group UK 01.06.2017 Nature Publishing Group Nature Portfolio
Subjects:	1-Phosphatidylinositol 3-kinase 631/80/86/2363 692/163/2743/137/773 82 82/80 96 96/1 96/106 96/109 96/31 Animals Cell Line Gene expression Glucagon Glucagon-like peptide 1 Glucagon-Like Peptide-1 Receptor - metabolism Glucose Glucose - metabolism Glycolysis Humanities and Social Sciences Hypoxia Hypoxia-inducible factor 1 Hypoxia-Inducible Factor 1, alpha Subunit - metabolism Hypoxia-inducible factor 1a Hypoxia-inducible factors Insulin Insulin secretion Insulin-Secreting Cells - metabolism Kinases Male Metabolism Mice, Inbred C57BL Mitochondria - metabolism multidisciplinary Pancreas Phosphorylation Rats RNA, Messenger - metabolism Science Science (multidisciplinary) Secretion Signal Transduction Stimulus-secretion coupling TOR protein TOR Serine-Threonine Kinases - metabolism Up-Regulation
ISSN:	2045-2322, 2045-2322
Online Access:	Get full text
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