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García-Cáceres, C. ; Quarta, C. ; Varela, L.* ; Gao, Y. ; Gruber, T. ; Legutko, B. ; Jastroch, M. ; Johansson, P.A. ; Ninkovic, J. ; Yi, C.-X. ; Le Thuc, O. ; Szigeti-Buck, K.* ; Cai, W.* ; Meyer, C.W. ; Pfluger, P.T. ; Fernandez, A.M.* ; Luquet, S.* ; Woods, S.C.* ; Torres-Alemán, I.* ; Kahn, C.R.* ; Götz, M. ; Horvath, T.L.* ; Tschöp, M.H.

Astrocytic insulin signaling couples brain glucose uptake with nutrient availability.

Cell 166, 867-880 (2016)
Verlagsversion Anhang DOI PMC
Open Access Green möglich sobald Postprint bei der ZB eingereicht worden ist.
We report that astrocytic insulin signaling co-regulates hypothalamic glucose sensing and systemic glucose metabolism. Postnatal ablation of insulin receptors (IRs) in glial fibrillary acidic protein (GFAP)-expressing cells affects hypothalamic astrocyte morphology, mitochondrial function, and circuit connectivity. Accordingly, astrocytic IR ablation reduces glucose-induced activation of hypothalamic pro-opio-melanocortin (POMC) neurons and impairs physiological responses to changes in glucose availability. Hypothalamus-specific knockout of astrocytic IRs, as well as postnatal ablation by targeting glutamate aspartate transporter (GLAST)-expressing cells, replicates such alterations. A normal response to altering directly CNS glucose levels in mice lacking astrocytic IRs indicates a role in glucose transport across the blood-brain barrier (BBB). This was confirmed in vivo in GFAP-IR KO mice by using positron emission tomography and glucose monitoring in cerebral spinal fluid. We conclude that insulin signaling in hypothalamic astrocytes co-controls CNS glucose sensing and systemic glucose metabolism via regulation of glucose uptake across the BBB.
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Publikationstyp Artikel: Journalartikel
Dokumenttyp Wissenschaftlicher Artikel
Schlagwörter Astrocytes ; Glucose Uptake ; Hypothalamus ; Insulin Receptor; Body-weight; Neuronal Dysfunction; Alzheimers-disease; Energy-metabolism; Barrier; Leptin; Cells; Transporter; Circuits; Mice
Sprache englisch
Veröffentlichungsjahr 2016
HGF-Berichtsjahr 2016
ISSN (print) / ISBN 0092-8674
e-ISSN 1097-4172
Zeitschrift Cell
Quellenangaben Band: 166, Heft: 4, Seiten: 867-880 Artikelnummer: , Supplement: ,
Verlag Cell Press
Verlagsort Cambridge, Mass.
Begutachtungsstatus Peer reviewed
Institut(e) Institute of Diabetes and Obesity (IDO)
Institute of Stem Cell Research (ISF)
POF Topic(s) 30201 - Metabolic Health
90000 - German Center for Diabetes Research
30204 - Cell Programming and Repair
Forschungsfeld(er) Helmholtz Diabetes Center
Stem Cell and Neuroscience
PSP-Element(e) G-502200-001
G-501900-221
G-500800-001
G-502294-001
DOI 10.1016/j.cell.2016.07.028
WOS ID WOS:000382258700011
Scopus ID 84981295660
PubMed ID 27518562
Erfassungsdatum 2016-09-02
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