open access

Vol 49, No 2 (2011)
ORIGINAL PAPERS
Published online: 2011-07-11
Submitted: 2011-12-19
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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 Demir
DOI: 10.5603/FHC.2011.0045
·
Folia Histochem Cytobiol 2011;49(2):325-334.

open access

Vol 49, No 2 (2011)
ORIGINAL PAPERS
Published online: 2011-07-11
Submitted: 2011-12-19

Abstract

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)

Abstract

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)
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Keywords

placental development; diabetes; glucocorticoid receptor; glucose transport

About this article
Title

Expression of glucocorticoid receptor and glucose transporter-1 during placental development in the diabetic rat

Journal

Folia Histochemica et Cytobiologica

Issue

Vol 49, No 2 (2011)

Pages

325-334

Published online

2011-07-11

DOI

10.5603/FHC.2011.0045

Bibliographic record

Folia Histochem Cytobiol 2011;49(2):325-334.

Keywords

placental development
diabetes
glucocorticoid receptor
glucose transport

Authors

Emin Türkay Korgun
Nuray Acar
Leyla Sati
Dijle Kipmen-Korgun
Asl Ozen
Gozde Unek
Ismail Ustunel
Ramazan Demir

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