TY - JOUR
T1 - Glucose transporter proteins in brain
T2 - Delivery of glucose to neurons and glia
AU - Vannucci, Susan J.
AU - Maher, Fran
AU - Simpson, Ian A.
N1 - Copyright:
Copyright 2007 Elsevier B.V., All rights reserved.
PY - 1997/9
Y1 - 1997/9
N2 - Glucose is the principle energy source for the mammalian brain. Delivery of glucose from the blood to the brain requires transport across the endothelial cells of the blood-brain barrier and into the neurons and glia. The facilitative glucose transporter proteins mediate these processes. The primary isoforms in brain are GLUT1, detected at high concentrations as a highly glycosylated form, (55 kDa) in blood-brain barrier, and also as a less glycosylated, 45 kDa form, present in parenchyma, predominantly glia; GLUT3 in neurons; and GLUT5 in microglia. The rest of the transporter family, GLUTs 2, 4, and 7, have also been detected in brain but at lower levels of expression and confined to more discrete regions. All of the transporters probably contribute to cerebral glucose utilization, as part of overall metabolism and metabolic interactions among cells. We discuss the properties, regulation, cell-specific location, and kinetic characteristics of the isoforms, their potential contributions to cerebral metabolism, and several experimental paradigms in which alterations in energetic demand and/or substrate supply affect glucose transporter expression.
AB - Glucose is the principle energy source for the mammalian brain. Delivery of glucose from the blood to the brain requires transport across the endothelial cells of the blood-brain barrier and into the neurons and glia. The facilitative glucose transporter proteins mediate these processes. The primary isoforms in brain are GLUT1, detected at high concentrations as a highly glycosylated form, (55 kDa) in blood-brain barrier, and also as a less glycosylated, 45 kDa form, present in parenchyma, predominantly glia; GLUT3 in neurons; and GLUT5 in microglia. The rest of the transporter family, GLUTs 2, 4, and 7, have also been detected in brain but at lower levels of expression and confined to more discrete regions. All of the transporters probably contribute to cerebral glucose utilization, as part of overall metabolism and metabolic interactions among cells. We discuss the properties, regulation, cell-specific location, and kinetic characteristics of the isoforms, their potential contributions to cerebral metabolism, and several experimental paradigms in which alterations in energetic demand and/or substrate supply affect glucose transporter expression.
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U2 - 10.1002/(SICI)1098-1136(199709)21:1<2::AID-GLIA2>3.0.CO;2-C
DO - 10.1002/(SICI)1098-1136(199709)21:1<2::AID-GLIA2>3.0.CO;2-C
M3 - Article
C2 - 9298843
AN - SCOPUS:0031238676
SN - 0894-1491
VL - 21
SP - 2
EP - 21
JO - Glia
JF - Glia
IS - 1
ER -