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Open Access Green as soon as Postprint is submitted to ZB.
The insulin-like growth factor I receptor regulates glucose transport by astrocytes.
Glia 64, 1962-1971 (2016)
Previous findings indicate that reducing brain insulin-like growth factor I receptor (IGF-IR) activity promotes ample neuroprotection. We now examined a possible action of IGF-IR on brain glucose transport to explain its wide protective activity, as energy availability is crucial for healthy tissue function. Using (18) FGlucose PET we found that shRNA interference of IGF-IR in mouse somatosensory cortex significantly increased glucose uptake upon sensory stimulation. In vivo microscopy using astrocyte specific staining showed that after IGF-IR shRNA injection in somatosensory cortex, astrocytes displayed greater increases in glucose uptake as compared to astrocytes in the scramble-injected side. Further, mice with the IGF-IR knock down in astrocytes showed increased glucose uptake in somatosensory cortex upon sensory stimulation. Analysis of underlying mechanisms indicated that IGF-IR interacts with glucose transporter 1 (GLUT1), the main facilitative glucose transporter in astrocytes, through a mechanism involving interactions with the scaffolding protein GIPC and the multicargo transporter LRP1 to retain GLUT1 inside the cell. These findings identify IGF-IR as a key modulator of brain glucose metabolism through its inhibitory action on astrocytic GLUT1 activity. GLIA 2016.
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Publication type
Article: Journal article
Document type
Scientific Article
Keywords
Astrocytes ; Glucose Metabolism ; Glucose Transporter 1 ; Insulin Like Growth Factor I Receptor
Language
english
Publication Year
2016
HGF-reported in Year
2016
ISSN (print) / ISBN
0894-1491
e-ISSN
1098-1136
Journal
Glia
Quellenangaben
Volume: 64,
Issue: 11,
Pages: 1962-1971
Publisher
Wiley
Reviewing status
Peer reviewed
Institute(s)
Institute of Diabetes and Obesity (IDO)
POF-Topic(s)
30201 - Metabolic Health
Research field(s)
Helmholtz Diabetes Center
PSP Element(s)
G-502200-001
PubMed ID
27462832
Erfassungsdatum
2016-09-06