Expression of glucocorticoid receptor and glucose transporter-1 during placental development in the diabetic rat
Emin Türkay Korgun, Nuray Acar, Leyla Sati, Dijle Kipmen-Korgun, Asl Ozen, Gozde Unek, Ismail Ustunel, Ramazan DemirFull Text:
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In various tissues, glucocorticoids (GCs) are known to downregulate glucose transport systems;
however, their effects on glucose transporters (GLUTs) in the placenta of a diabetic rat are unknown. Glucocorticoid
hormone action within the cell is regulated by the glucocorticoid receptor (GR). Thus, this study was
designed to investigate the relationship between GR and glucose transporter expression in the placenta of the
diabetic rat. Our immunohistochemical results indicated that GR and glucose transporter protein 1 (GLUT 1)
are expressed ubiquitously in the trophoblast and endothelial cells of the labyrinthine zone, where maternal
fetal transport takes place in the rat placenta. Expression of GR in the junctional zone of the rat placenta was
detected in giant cells, and in some spongiotrophoblast cells, but not in the glycogen cells. GLUT 1 was present,
especially in glycogen cells during early pregnancy, and in the spongiotrophoblast cells of the junctional zone
during late pregnancy. Amounts of GR and GLUT 1 protein were increased towards the end of gestation both
in the control and the diabetic placenta. However, at days 17 and 19 of gestation, only the placental GR
protein was significantly increased in the streptozotocin-induced diabetic rats compared to control rats. Diabetes
led to a significant decrease in placental weight at gestation day 15. In contrast, at gestational days 17
and 21, the weights of the diabetic placenta were significantly increased as compared with the controls. Moreover,
diabetes induced fetus intrauterine growth retardation at gestational days 13, 17 and 21. In conclusion,
the localization pattern of GR and GLUT 1 proteins in the same cell types led us to believe that there might be
a relationship between GR and GLUT 1 expressions at the cellular level. GLUT 1 does not play a pivotal role
in diabetic pregnancies. However, placental growth abnormalities during diabetic pregnancy may be related to
the amount of GR. (Folia Histochemica et Cytobiologica 2011; Vol. 49, No. 2, pp. 325–334)
however, their effects on glucose transporters (GLUTs) in the placenta of a diabetic rat are unknown. Glucocorticoid
hormone action within the cell is regulated by the glucocorticoid receptor (GR). Thus, this study was
designed to investigate the relationship between GR and glucose transporter expression in the placenta of the
diabetic rat. Our immunohistochemical results indicated that GR and glucose transporter protein 1 (GLUT 1)
are expressed ubiquitously in the trophoblast and endothelial cells of the labyrinthine zone, where maternal
fetal transport takes place in the rat placenta. Expression of GR in the junctional zone of the rat placenta was
detected in giant cells, and in some spongiotrophoblast cells, but not in the glycogen cells. GLUT 1 was present,
especially in glycogen cells during early pregnancy, and in the spongiotrophoblast cells of the junctional zone
during late pregnancy. Amounts of GR and GLUT 1 protein were increased towards the end of gestation both
in the control and the diabetic placenta. However, at days 17 and 19 of gestation, only the placental GR
protein was significantly increased in the streptozotocin-induced diabetic rats compared to control rats. Diabetes
led to a significant decrease in placental weight at gestation day 15. In contrast, at gestational days 17
and 21, the weights of the diabetic placenta were significantly increased as compared with the controls. Moreover,
diabetes induced fetus intrauterine growth retardation at gestational days 13, 17 and 21. In conclusion,
the localization pattern of GR and GLUT 1 proteins in the same cell types led us to believe that there might be
a relationship between GR and GLUT 1 expressions at the cellular level. GLUT 1 does not play a pivotal role
in diabetic pregnancies. However, placental growth abnormalities during diabetic pregnancy may be related to
the amount of GR. (Folia Histochemica et Cytobiologica 2011; Vol. 49, No. 2, pp. 325–334)
Keywords
placental development; diabetes; glucocorticoid receptor; glucose transport
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