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


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Korgun E. T., Acar N., Sati L., Kipmen-Korgun D., Ozen A., Unek G., ...Daha Fazla

FOLIA HISTOCHEMICA ET CYTOBIOLOGICA, cilt.49, sa.2, ss.325-334, 2011 (SCI-Expanded) identifier identifier identifier

  • Yayın Türü: Makale / Tam Makale
  • Cilt numarası: 49 Sayı: 2
  • Basım Tarihi: 2011
  • Doi Numarası: 10.5603/fhc.2011.0045
  • Dergi Adı: FOLIA HISTOCHEMICA ET CYTOBIOLOGICA
  • Derginin Tarandığı İndeksler: Science Citation Index Expanded (SCI-EXPANDED), Scopus
  • Sayfa Sayıları: ss.325-334
  • Anahtar Kelimeler: placental development, diabetes, glucocorticoid receptor, glucose transport, 11-BETA-HYDROXYSTEROID DEHYDROGENASE TYPE-2, GLUCOSE-TRANSPORTER, NUTRIENT TRANSPORT, FETAL-GROWTH, INSULIN, CORTICOSTERONE, DEXAMETHASONE, PROGESTERONE, PREGNANCY, BARRIER
  • Akdeniz Üniversitesi Adresli: Evet

Özet

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.