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Fuente-Martin, E. ; García-Cáceres, C. ; Argente-Arizon, P.* ; Díaz, F.* ; Granado, M.* ; Freire-Regatillo, A.* ; Castro-Gonzalez, D.* ; Ceballos, M.L.* ; Frago, L.M.* ; Dickson, S.L.* ; Argente, J.* ; Chowen, J.A.*

Ghrelin regulates glucose and glutamate transporters in hypothalamic astrocytes.

Sci. Rep. 6:23673 (2016)
Verlagsversion DOI
Open Access Gold
Creative Commons Lizenzvertrag
Hypothalamic astrocytes can respond to metabolic signals, such as leptin and insulin, to modulate adjacent neuronal circuits and systemic metabolism. Ghrelin regulates appetite, adiposity and glucose metabolism, but little is known regarding the response of astrocytes to this orexigenic hormone. We have used both in vivo and in vitro approaches to demonstrate that acylated ghrelin (acyl-ghrelin) rapidly stimulates glutamate transporter expression and glutamate uptake by astrocytes. Moreover, acyl-ghrelin rapidly reduces glucose transporter (GLUT) 2 levels and glucose uptake by these glial cells. Glutamine synthetase and lactate dehydrogenase decrease, while glycogen phosphorylase and lactate transporters increase in response to acyl-ghrelin, suggesting a change in glutamate and glucose metabolism, as well as glycogen storage by astrocytes. These effects are partially mediated through ghrelin receptor 1A (GHSR-1A) as astrocytes do not respond equally to desacyl-ghrelin, an isoform that does not activate GHSR-1A. Moreover, primary astrocyte cultures from GHSR-1A knock-out mice do not change glutamate transporter or GLUT2 levels in response to acyl-ghrelin. Our results indicate that acyl-ghrelin may mediate part of its metabolic actions through modulation of hypothalamic astrocytes and that this effect could involve astrocyte mediated changes in local glucose and glutamate metabolism that alter the signals/nutrients reaching neighboring neurons.
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Publikationstyp Artikel: Journalartikel
Dokumenttyp Wissenschaftlicher Artikel
Schlagwörter Body-weight; Food-intake; Differential Expression; Primary Cultures; Arcuate Nucleus; Brain; Neurons; Obesity; Metabolism; Activation
ISSN (print) / ISBN 2045-2322
e-ISSN 2045-2322
Zeitschrift Scientific Reports
Quellenangaben Band: 6, Heft: , Seiten: , Artikelnummer: 23673 Supplement: ,
Verlag Nature Publishing Group
Verlagsort London
Begutachtungsstatus Peer reviewed