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The Journal of Clinical Endocrinology & Metabolism Vol. 84, No. 4 1445-1452
Copyright © 1999 by The Endocrine Society

Original Studies

Placental Glucose Transporter Expression Is Regulated by Glucocorticoids1

T. Hahn, S. Barth, R. Graf, M. Engelmann, D. Beslagic, J. M. H. M. Reul, F. Holsboer, G. Dohr and G. Desoye

Institute of Histology and Embryology (T.H., G.Do.) and the Institute of Hygiene (S.B.), University of Graz, A-8010 Graz, Austria; the Department of Obstetrics and Gynecology, University of Graz Medical School (T.H., G.De.), A-8036 Graz, Austria; the Institute of Anatomy, Free University of Berlin (R.G.), D-14195 Berlin, Germany; Max Planck Institute of Psychiatry (M.E., J.M.R., F.H.), D-80804 Munich, Germany; and the Department of Medicine, University of Queensland, Royal Brisbane Hospital (D.B.), Herston, Queensland 4029, Australia

Address all correspondence and requests for reprints to: Dr. Tom Hahn, Institute of Histology and Embryology, University of Graz, Harrachgasse 21, A-8010 Graz, Austria. E-mail: tom.hahn{at}kfunigraz.ac.at

Although glucocorticoids play important roles in development and fetal programming, they are widely used for treatment of a variety of diseases during pregnancy. In various tissues, glucocorticoids down-regulate glucose transport systems; however, their effects on glucose transporters in the placenta are unknown. In the present study, the glucose carrier proteins GLUT1 and GLUT3 were localized in the trophoblast and endothelium of the human, rat, and mouse placenta. Subsequently, it was investigated whether glucocorticoids affect messenger ribonucleic acid and protein expression of these molecules by Northern and Western blotting using 1) human term placental trophoblast cells cultured in the presence or absence of 0.5, 5, and 50 µmol/L triamcinolone; 2) placentas of rats that received a single ip dose of 0.38 mg/kg triamcinolone; and 3) placentas of transgenic mice bearing an antisense glucocorticoid receptor gene construct. In all of these systems, both glucose transporters were significantly down-regulated (P < 0.05), with the exception of increased GLUT3 messenger ribonucleic acid and protein levels in transgenic mice. The results demonstrate that triamcinolone is a potent regulator of placental GLUT1 and GLUT3 expression involving the glucocorticoid receptor. We speculate that impaired expression of placental glucose transporters after glucocorticoid administration might contribute to the adverse side-effects, the foremost of which is a growth-retarded fetus, of this treatment during pregnancy.




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