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Alteration of glucose metabolism in cultured astrocytes after AQP9-small interference RNA application


Badaut, J; Brunet, J F; Guérin, C; Regli, L; Pellerin, L (2012). Alteration of glucose metabolism in cultured astrocytes after AQP9-small interference RNA application. Brain Research, 1473:19-24.

Abstract

Aquaglyceroporin-9 (AQP9) facilitates diffusion of water and energy substrates such as glycerol and monocarboxylates. AQP9 is present in plasma membrane and mitochondria of astrocytes and catecholaminergic neurons, suggesting that it plays a role in the energetic status of these cells. Using specific small interference RNA directed against AQP9 in astrocyte cultures, we showed that glycerol uptake is decreased which is associated with an increase in glucose uptake and oxidative metabolism. Our results not only confirm the presence of AQP9 in astrocytes but also suggest that changes in AQP9 expression alter glial energy metabolism.

Abstract

Aquaglyceroporin-9 (AQP9) facilitates diffusion of water and energy substrates such as glycerol and monocarboxylates. AQP9 is present in plasma membrane and mitochondria of astrocytes and catecholaminergic neurons, suggesting that it plays a role in the energetic status of these cells. Using specific small interference RNA directed against AQP9 in astrocyte cultures, we showed that glycerol uptake is decreased which is associated with an increase in glucose uptake and oxidative metabolism. Our results not only confirm the presence of AQP9 in astrocytes but also suggest that changes in AQP9 expression alter glial energy metabolism.

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Additional indexing

Item Type:Journal Article, refereed, original work
Communities & Collections:04 Faculty of Medicine > University Hospital Zurich > Clinic for Neurosurgery
Dewey Decimal Classification:610 Medicine & health
Scopus Subject Areas:Life Sciences > General Neuroscience
Life Sciences > Molecular Biology
Health Sciences > Neurology (clinical)
Life Sciences > Developmental Biology
Language:English
Date:14 September 2012
Deposited On:21 Mar 2013 12:38
Last Modified:09 Nov 2023 02:45
Publisher:Elsevier
ISSN:0006-8993
OA Status:Closed
Publisher DOI:https://doi.org/10.1016/j.brainres.2012.07.041
PubMed ID:22842525
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