期刊
BRAIN RESEARCH
卷 904, 期 1, 页码 20-30出版社
ELSEVIER SCIENCE BV
DOI: 10.1016/S0006-8993(01)02418-0
关键词
brain metabolism; epilepsy; GLUT-1; hexokinase; in vitro models; tight junctions
资金
- NHLBI NIH HHS [2RO1 HL51614] Funding Source: Medline
- NINDS NIH HHS [R01 NS38195] Funding Source: Medline
How the brain meets its continuous high metabolic demand in light of varying plasma glucose levels and a functional blood-brain barrier (BBB) is poorly understood. GLUT-1, found in high density at the BBB appears to maintain the continuous shuttling of glucose across the blood-brain barrier irrespective of the plasma concentration. We examined the process of glucose transport across a quasi-physiological in vitro blood-brain barrier model. Radiolabeled tracer permeability studies revealed a concentration ratio of abluminal to luminal glucose in this blood-brain barrier model of approximately 0.85. Under conditions where [glucose](lumen) was higher than [glucose](ablumen), influx of radiolabeled 2-deoxyglucose from lumen to the abluminal compartment was approximately 35% higher than efflux from the abluminal side to the lumen. However, when compartmental [glucose] were maintained equal, a reversal of this trend was seen (approximately 19% higher efflux towards the lumen), favoring establishment of a luminal to abluminal concentration gradient. Immunocytochemical experiments revealed that in addition to segregation of GLUT-1 (luminal > abluminal), the intracellular enzyme hexokinase was also asymmetrically distributed (abluminal > luminal). We conclude that glucose transport at the CNS/blood interface appears to be dependent on and regulated by a serial chain of membrane-bound and intracellular transporters and enzymes. (C) 2001 Published by Elsevier Science B.V.
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