Glucose transporter expression in brain: Relationship to cerebral glucose utilization

被引:130
作者
Vannucci, SJ
Clark, RR
Koehler-Stec, E
Li, K
Smith, CB
Davies, P
Maher, F
Simpson, IA
机构
[1] NIDDK, Diabet Branch, NIH, Bethesda, MD 20892 USA
[2] Penn State Univ, Milton S Hershey Med Ctr, Dept Pediat, Hershey, PA 17033 USA
[3] NIMH, Cerebral Metab Lab, NIH, Bethesda, MD 20892 USA
[4] Albert Einstein Coll Med, Dept Pathol, Bronx, NY 10467 USA
关键词
glucose transport; cerebral glucose utilization; neurons; glia; Alzheimer's disease; cerebral development; dehydration;
D O I
10.1159/000017333
中图分类号
Q [生物科学];
学科分类号
07 ; 0710 ; 09 ;
摘要
Glucose is the principle energy source for mammalian brain. Delivery of glucose from the blood to the brain requires its transport across the endothelial cells of the blood-brain barrier and across the plasma membranes of neurons and glia, which is mediated by the facilitative glucose transporter proteins. The two primary glucose transporter isoforms which function in cerebral glucose metabolism are GLUT1 and GLUT3. GLUT1 is the primary transporter in the blood-brain barrier, choroid plexus, ependyma, and glia; GLUT3 is the neuronal glucose transporter. The levels of expression of both transporters are regulated in concert with metabolic demand and regional rates of cerebral glucose utilization. We present several experimental paradigms in which alterations in energetic demand and/or substrate supply affect glucose transporter expression. These include normal cerebral development in the rat, Alzheimer's disease, neuronal differentiation in vitro, and dehydration in the rat.
引用
收藏
页码:369 / 379
页数:11
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