Subcellular distribution of glucose transporter (GLUT-1) during development of the blood-brain barrier in rats

1996 ◽  
Vol 284 (3) ◽  
pp. 355-365 ◽  
Author(s):  
Sylvia Bolz ◽  
Catherine L. Farrell ◽  
Klaus Dietz ◽  
Hartwig Wolburg
Keyword(s):  
Blood Brain Barrier ◽  
Subcellular Distribution ◽  
Glucose Transporter ◽  
Brain Barrier ◽  
Glut 1 ◽  
Blood Brain

Changes in the glucose transporter of brain capillaries

1992 ◽  
Vol 70 (S1) ◽  
pp. S113-S117 ◽  
Author(s):  
Sami I. Harik
Keyword(s):  
Alzheimer Disease ◽  
Blood Brain Barrier ◽  
Glucose Transporter ◽  
Glucose Transporters ◽  
Brain Barrier ◽  
Capillary Endothelium ◽  
Brain Capillaries ◽  
Glut 1 ◽  
Blood Brain ◽  
The Brain

Brain capillary endothelium has a high density of the GLUT-1 facilitative glucose transporter protein. This is reasonable in view of the brain's high metabolic rate for glucose and its isolation behind unique capillaries with blood – brain barrier properties. Thus, the brain endothelium, which constitutes less than 0.1% of the brain weight, has to transport glucose for the much larger mass of surrounding neurons and glia. I describe here the changes that occur in the density of glucose transporters in brain capillaries of subjects with Alzheimer disease, where there is a decreased cerebral metabolic rate for glucose, and in a novel clinical entity characterized by defective glucose transport at the blood – brain barrier. In subjects with Alzheimer disease, cerebral microvessels showed a marked decrease in the density of the glucose transporter when compared with age-matched controls, but there was no change in the density of glucose transporters in erythrocyte membranes. Thus, I believe that the decreased density of glucose transporters in the brains of subjects with Alzheimer disease is the result rather than the cause of the disease. In contradistinction, the primary defect in glucose transport at the blood – brain barrier in subjects with the recently described entity is associated with decreased density of GLUT-1 in erythrocyte membranes.Key words: brain microvessels, capillary endothelium, blood – brain barrier, glucose transporter, Alzheimer disease, hypoglycorrhachia.

17 beta-Estradiol modulation of glucose transporter 1 expression in blood-brain barrier

1997 ◽  
Vol 272 (6) ◽  
pp. E1016-E1022 ◽  
Author(s):  
J. Shi ◽  
J. W. Simpkins
Keyword(s):  
Endothelial Cells ◽  
Blood Brain Barrier ◽  
Glucose Transporter ◽  
Northern Blotting ◽  
Female Rats ◽  
Brain Barrier ◽  
Glucose Transporter 1 ◽  
Glut 1 ◽  
Blood Brain

The present study was designed to evaluate 17 beta-estradiol (E2) modulation of glucose transporter 1 (GLUT-1) protein and mRNA expression in blood-brain barrier (BBB) endothelium. Female rats were ovariectomized (OVX) for 12-14 days, then E2 was injected at dosages of 1-100 micrograms/kg sc at 2-16 h before sampling. Glucose transport into BBB endothelial cells was assessed using 2-deoxy-[14C]glucose (2-[14C]DG) uptake. GLUT-1 protein and mRNA samples were analyzed by Western and Northern blotting, respectively. E2 treatment caused dose- and time-dependent increases in 2-[14C]DG uptake and GLUT-1 protein expression by microvessels. The peak responses were induced by 10 micrograms/kg E2 dose at the 4-h sampling time (36.0 and 31.3% increases, P < 0.05, respectively). GLUT-1 mRNA demonstrated a transient increase at 15 min (55%, P < 0.05), then decreased to basal level by 2 h. This study shows that in vivo treatment with E2 increases 2-[14C]DG uptake into the BBB endothelial cells and suggests this E2 effect is due to its modulation of GLUT-1 mRNA and protein.

Glucose transport by isolated plasma membranes of the bovine blood-brain barrier

1997 ◽  
Vol 272 (5) ◽  
pp. C1552-C1557 ◽  
Author(s):  
W. J. Lee ◽  
D. R. Peterson ◽  
E. J. Sukowski ◽  
R. A. Hawkins
Keyword(s):  
Glucose Transport ◽  
Blood Brain Barrier ◽  
Plasma Membranes ◽  
Glucose Transporter ◽  
Extracellular Fluid ◽  
Brain Barrier ◽  
Maximal Velocity ◽  
Plasma Membrane Vesicles ◽  
Cerebral Microvessels ◽  
Blood Brain

Luminal and abluminal endothelial plasma membrane vesicles were isolated from bovine cerebral microvessels, the site of the blood-brain barrier. Glucose transport across each membrane was measured using a rapid-filtration technique. Glucose transport into luminal vesicles occurred by a stereospecific energy-independent transporter [Michaelis-Menten constant (K(m)) = 10.3 +/- 2.8 (SE) mM and maximal velocity (Vmax) = 8.6 +/- 2.0 nmol.mg protein(-1).min-1]. Kinetic analysis of abluminal vesicles also showed a transport system with characteristics similar to the luminal transporter (K(m) = 12.5 +/- 2.3 mM and Vmax = 10.0 +/- 1.0 nmol.mg protein-1.min-1). These functional, facilitative glucose transporters were symmetrically distributed between the luminal and abluminal membrane domains, providing a mechanism for glucose movement between blood and brain. The studies also revealed a Na-dependent transporter on the abluminal membrane with a higher affinity and lower capacity than the facilitative transporters (K(m) = 130 +/- 20 microM and Vmax = 1.59 +/- 0.44 nmol.mg protein-1.min-1. The abluminal Na-dependent glucose transporter is in a position to transport glucose from the brain extracellular fluid into the endothelial cells of the blood-brain barrier. The functional significance of its presence there remains to be determined.

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