Human Reproduction, Vol 13, 799-804, Copyright © 1998 by Oxford University Press
M Shams, MD Kilby, DA Somerset, AJ Howie, A Gupta, PJ Wood, M Afnan and PM Stewart
The type 2 isoform of 11beta-hydroxysteroid dehydrogenase (11beta- HSD2),
which inactivates cortisol (F) to cortisone (E), has been suggested to play
a role in the ontogeny of the fetal pituitary-adrenal axis and also protect
the developing fetus from the deleterious effects of circulating maternal
glucocorticoids. The abundance of 11beta-HSD2 in the placenta and other
fetal tissues was inferred from the F/E ratio in 17 term deliveries in both
umbilical arterial (1.73 +/- 0.24, mean +/- SE) and umbilical venous blood
(1.16 +/- 0.14) compared with adult peripheral venous blood (7.76 +/- 0.57,
n = 70). Using sensitive assays for 11beta-HSD2 and an in-house human
11beta-HSD2 antibody, the expression and activity of this enzyme in fresh
frozen human placenta increased progressively from first (8-12 weeks, n =
16) and second (13- 20 weeks, n = 9) to third trimester (term) pregnancies
(39-40 weeks, n = 50). Placental 11beta-HSD2 activity was significantly
reduced in deliveries complicated by intrauterine growth restriction (IUGR)
[25-36 weeks, n = 12, activity 380 pmol/mg/h median (225-671; 95%
confidence interval)], compared with the term deliveries [888 (725-1362)]
and with appropriately grown pre-term deliveries [27-36 weeks, n = 14,
activity 810 (585-1269)], P < 0.05. In human pregnancy placental
11beta-HSD2 activity increases markedly in the third trimester of pregnancy
at a time when maternal circulating levels of glucocorticoid are rising.
The finding of attenuated placental 11beta-HSD2 activity in IUGR suggests
that glucocorticoids may, in part, contribute to impaired fetal growth and
that this is closely controlled in normal gestation through placental
11beta-HSD2 expression.
ARTICLES
11Beta-hydroxysteroid dehydrogenase type 2 in human pregnancy and reduced expression in intrauterine growth restriction
Department of Medicine, Queen Elizabeth Hospital, University of Birmingham, Edgbaston, UK.
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