Placental glucose transporter expression is regulated by glucocorticoids

Although glucocorticoids play important roles in development and fetal prog ramming, they are widely used for treatment of a variety of diseases during pregnancy. In various tissues, glucocorticoids downregulate glucose transp ort 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 glucocorticoi ds affect messenger ribonucleic acid and protein expression of these molecu les by Northern and Western blotting using 1) human term placental trophobl ast cells cultured in the presence or absence of 0.5, 5, and 50 mu mol/L tr iamcinolone; 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 gluc ose transporters were significantly downregulated (P < 0.05), with the exce ption of increased GLUT3 messenger ribonucleic acid and protein levels in t ransgenic mice. The results demonstrate that triamcinolone is a potent regu lator of placental GLUT1 and GLUT3 expression involving the glucocorticoid receptor. We speculate that impaired expression of placental glucose transp orters after glucocorticoid administration might contribute to the adverse side-effects, the foremost of which is a growth-retarded fetus, of this tre atment during pregnancy.