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Am J Physiol Endocrinol Metab 272: E1016-E1022, 1997;
0193-1849/97 $5.00
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AJP - Endocrinology and Metabolism, Vol 272, Issue 6 E1016-E1022, Copyright © 1997 by American Physiological Society


ARTICLES

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

J. Shi and J. W. Simpkins
Center for the Neurobiology of Aging, College of Pharmacy, University of Florida, Gainesville 32610, USA.

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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