Glucocorticoids, feto-placental 11β-hydroxysteroid dehydrogenase type 2, .and the early life origins of adult disease

摘要

Increasing human epidemiological data suggest that events that subtly retard intrauterine growth may determine common disorders, such as hypertension and non-insulin-dependent diabetes, in adult life. The underlying mechanisms are unknown. However, excessive fetal exposure to glucocorticoids retards growth and "programs" adult hypertension in rats.11β-Hydroxysteroid dehydrogenase type 2(11β-HSD2) catalyzes the rapid inacti- vation of cortisol and corticosterone to inert 11 keto-products. Normally, 11β-HSD2 in the placenta and some fetal tissues is thought to protect the fetus from excess maternal glucocorticoids.