Differences in expression and activity of 11beta-hydroxysteroid dehydrogenase type 1 and 2 in human placentas of term pregnancies according to birth weight and gender

Eur J Endocrinol. 2009 Sep;161(3):419-25. doi: 10.1530/EJE-09-0308. Epub 2009 Jun 19.

Abstract

Background: Fetal exposure to maternal glucocorticoids may determine fetal growth and the programing of later disorders. Availability of the glucocorticoids in the placenta is regulated by the 11beta-hydroxysteroid dehydrogenase (11beta-HSDs) enzymes. To date, there are discrepancies with regard to cortisol (F) cord blood levels in fetuses with intrauterine growth retardation in different species. Objective To study the expression and activity of 11beta-HSDs in placentas from full term small for gestational age (SGA), appropriate for gestational age (AGA) and large for gestational age (LGA) newborns, and cortisol cord blood concentration.

Methods: Twenty-five placentas from AGA, 24 SGA and 25 LGA were collected.

Results: SGA newborns had significantly lower and LGA newborns had significantly higher birth weight, birth length, head circumference, and placental weight than AGA counterparts. We observed a direct correlation between placental weight and birth weight, birth length and head circumference, and higher cord F levels in SGA newborns. The 11beta-HSD1 expression was similar among the SGA, AGA, and LGA placentas. However, within the placentas of SGA newborns, the 11beta-HSD1 mRNA levels were significantly reduced in the chorionic plate compared with basal plate. An inverse correlation between cord F levels and activity of 11beta-HSD1 in the chorionic plate of the SGA placentas was detected. The 11beta-HSD2 activity was seven- to eightfold higher compared with 11beta-HSD1 in the placentas, and there was a lower 11beta-HSD2 activity in females' SGA placentas compared with the male SGA placentas.

Conclusion: We observed a lower expression and activity of 11beta-HSD1 in the chorionic plate of the SGA placentas, suggesting a possible compensatory mechanism to diminish the higher cortisol fetal concentrations observed in fetuses with intrauterine growth restriction.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • 11-beta-Hydroxysteroid Dehydrogenase Type 1 / genetics*
  • 11-beta-Hydroxysteroid Dehydrogenase Type 1 / metabolism
  • 11-beta-Hydroxysteroid Dehydrogenase Type 2 / genetics*
  • 11-beta-Hydroxysteroid Dehydrogenase Type 2 / metabolism
  • Birth Weight / genetics*
  • Chorion / enzymology
  • Chorion / metabolism
  • Female
  • Fetal Growth Retardation / enzymology
  • Fetal Growth Retardation / genetics
  • Fetal Growth Retardation / metabolism
  • Gene Expression Regulation, Enzymologic
  • Gestational Age
  • Humans
  • Infant, Newborn
  • Infant, Small for Gestational Age / metabolism
  • Male
  • Placenta / metabolism*
  • Pregnancy
  • Pregnancy Trimester, Third / genetics*
  • Pregnancy Trimester, Third / metabolism
  • Sex Factors
  • Term Birth / genetics*
  • Term Birth / metabolism

Substances

  • 11-beta-Hydroxysteroid Dehydrogenase Type 1
  • 11-beta-Hydroxysteroid Dehydrogenase Type 2