scholarly journals Quantitative Immunocytochemical Study of Blood-Brain Barrier Glucose Transporter (GLUT-1) in Four Regions of Mouse Brain

1999 ◽  
Vol 47 (8) ◽  
pp. 1021-1030 ◽  
Author(s):  
Danuta H. Dobrogowska ◽  
Andrzej W. Vorbrodt
1996 ◽  
Vol 284 (3) ◽  
pp. 355-365 ◽  
Author(s):  
Sylvia Bolz ◽  
Catherine L. Farrell ◽  
Klaus Dietz ◽  
Hartwig Wolburg

1992 ◽  
Vol 70 (S1) ◽  
pp. S113-S117 ◽  
Author(s):  
Sami I. Harik

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.


1997 ◽  
Vol 272 (6) ◽  
pp. E1016-E1022 ◽  
Author(s):  
J. Shi ◽  
J. W. Simpkins

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.


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