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UID:DSC-14986
DTSTART;TZID=Europe/Berlin:20180927T110000
SEQUENCE:1536660543
TRANSP:OPAQUE
DTEND;TZID=Europe/Berlin:20180927T120000
URL:https://dresden-science-calendar.de/calendar/de/detail/14986
LOCATION:TUD CRTD\, Fetscherstraße 10501307 Dresden
SUMMARY:Newsholme: The importance of metabolic reprogramming to cell functi
 on
CLASS:PUBLIC
DESCRIPTION:Speaker: Philip Newsholme\nInstitute of Speaker: Curtin Univers
 ity Perth\, Curtin Health Innovation Research Institute\, Faculty of Healt
 h Sciences\, School of Pharmacy and Biomedical Sciences\nTopics:\nBiologie
 \, Medizin\n Location:\n  Name: TUD CRTD (Auditorium left)\n  Street: Fets
 cherstraße 105\n  City: 01307 Dresden\n  Phone: +49 (0)351 458 82052\n  F
 ax: +49 (0)351 458 82059 \nDescription: Glucagon-like-peptide-1 (GLP-1) pr
 omotes insulin secretion from pancreatic β-cells in a glucose dependent m
 anner. Several pathways mediate this action by rapid\, kinase phosphorylat
 ion-dependent\, but gene expression-independent mechanisms. GLP-1-induced 
 insulin secretion requires glucose metabolism\, therefore GLP-1 receptor (
 GLP-1R) signalling may impact glucose uptake and utilization in β-cells. 
 By determination of changes to various metabolic parameters after short an
 d long exposure of clonal BRIN-BD11 β-cells and rodent islets to the GLP-
 1R agonist Exendin-4 (50 nM)\, we found that prolonged stimulation of the 
 GLP-1R (18 hours) promoted metabolic reprogramming of β-cells. We determi
 ned up-regulation of glycolytic enzyme expression\, increased rates of glu
 cose uptake and consumption\, as well as augmented ATP content\, insulin s
 ecretion and glycolytic flux. In our model\, depletion of Hypoxia-Inducibl
 e Factor 1 alpha (HIF-1α) impaired the effects of Exendin-4 on glucose me
 tabolism\, while pharmacological inhibition of Phosphoinositide 3-kinase (
 PI3K) or mTOR completely abolished such effects. Considering the central r
 ole of glucose catabolism for stimulus-secretion coupling in β-cells\, ou
 r findings suggest that chronic GLP-1 actions on insulin secretion include
  elevated β-cell glucose metabolism.
DTSTAMP:20260615T041109Z
CREATED:20180911T100903Z
LAST-MODIFIED:20180911T100903Z
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