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Titolo:
Increased expression of neuronal glucose transporter 3 but not glial glucose transporter 1 following severe diffuse traumatic brain injury in rats
Autore:
Hamlin, GP; Cernak, I; Wixey, JA; Vink, R;
Indirizzi:
James Cook Univ N Queensland, Dept Physiol & Pharmacol, Townsville, Qld 4811, Australia James Cook Univ N Queensland Townsville Qld Australia 4811 811, Australia Univ Adelaide, Dept Pathol, Adelaide, SA 5001, Australia Univ Adelaide Adelaide SA Australia 5001 ol, Adelaide, SA 5001, Australia
Titolo Testata:
JOURNAL OF NEUROTRAUMA
fascicolo: 10, volume: 18, anno: 2001,
pagine: 1011 - 1018
SICI:
0897-7151(200110)18:10<1011:IEONGT>2.0.ZU;2-N
Fonte:
ISI
Lingua:
ENG
Soggetto:
GENE-EXPRESSION; ISCHEMIC-INJURY; GLUT1; HYPOGLYCEMIA; LOCALIZATION; DEPRIVATION; PROTEINS;
Keywords:
cerebellum; glucose transport; Glut1; Glut3; neurotrauma;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
39
Recensione:
Indirizzi per estratti:
Indirizzo: Hamlin, GP James Cook Univ N Queensland, Dept Physiol & Pharmacol, Townsville, Qld 4811, Australia James Cook Univ N Queensland Townsville Qld Australia 4811 lia
Citazione:
G.P. Hamlin et al., "Increased expression of neuronal glucose transporter 3 but not glial glucose transporter 1 following severe diffuse traumatic brain injury in rats", J NEUROTRAU, 18(10), 2001, pp. 1011-1018

Abstract

Traumatic brain injury results in an increased brain energy demand that isassociated with profound changes in brain glycolysis and energy metabolism. Increased glycolysis must be met by increasing glucose supply that, in brain, is primarily mediated by two members of the facilitative glucose transporter family, Glut1 and Glut3. Glut1 is expressed in endothelial cells of the blood-brain barrier (BBB) and also in glia, while Glut3 is the primary glucose transporter expressed in neurons. However, few studies have investigated the changes in glucose transporter expression following traumatic brain injury, and in particular, the neuronal and glial glucose transporter responses to injury. This study has therefore focussed on investigating the expression of the glial specific 45-kDa isoform of Glut1 and neuronal specific Glut3 following severe diffuse traumatic brain injury in rats. Followingimpact-acceleration injury, Glut3 expression was found to increase by at least 300% as early as 4 h after induction of injury and remained elevated for at least 48 h postinjury. The increase in Glut3 expression was clearly evident in both the cerebral cortex and cerebellum. In contrast, expression of the glial specific 45-kDa isoform of Glut1 did not significantly change in either the cerebral cortex or cerebellum following traumatic injury. We conclude that increased glucose uptake after traumatic brain injury is primarily accounted for by increased neuronal Glut 3 glucose transporter expression and that this increased expression after trauma is part of a neuronal stress response that may be involved in increasing neuronal glycolysis and associated energy metabolism to fuel repair processes.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 29/05/20 alle ore 09:39:05