Submitted to: Biology of Reproduction
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 3/12/1996
Publication Date: N/A
Citation: N/A Interpretive Summary: The steroid hormone cortisol is made and secreted into the blood by the adrenal gland. During pregnancy, cortisol from the maternal adrenal can pass through the placenta and into the fetus. It has been suggested for humans and rodents that the placental enzyme, a biological catalyst, 11beta-hydroxysteroid dehydrogenase (11B-HSD) converts biologically active cortisol to an inactive steroid, cortisone. Such an action would thereby protect the fetus from high cortisol concentrations that could slow fetal growth. Studies were conducted to determine 1) if 11B-HSD was present in pig placentae, 2) if its activity changed during gestation, and 3) if its activity was related (correlated) to fetal development. It was determined that 11B-HSD activity was present in pig placentae, and this activity increased steadily between 50 and 100 days of gestation (term = 114 days). There was a significant, positive correlation between placental 11B-HSD and dfetal length only at 75 days of gestation. The results suggest an association between placental 11B-HSD activity and fetal development in pigs that presumably acts by regulating the amount of biologically active cortisol to which the placenta and fetus are exposed.
Technical Abstract: The enzyme 11beta-hydroxysteroid dehydrogenase (11B-HSD) reversibly converts biologically active cortisol to inactive cortisone, and when present in placentae may act to protect fetuses from high concentrations of maternal glucocorticoids. Experiments were conducted to study porcine placental 11B-HSD oxidative activity (conversion of cortisol to cortisone). .Placentae were obtained at 50, 75, and 100 days of gestation from uterine environments that were "roomy" or "crowded" subsequent to uterine ligation on Day 2 of gestation. Fetal weight and length were increased (p </= .015) in roomy compared with the crowded uterine environment at each gestational age. Both NADP+ and NAD+-dependent 11B-HSD increased almost fivefold between 50 and 100 days of gestation (p<.02). At each gestational age NAD+- dependent 11B-HSD was over twofold greater (p<.001) than NADP+-dependent 11B-HSD. Significant statistical interactions among gestational age, uterine environment, and fetal sex indicate effects of these factors on placental 11B-HSD activity are complex. Correlations between placental 11B- HSD and fetal/placental size were few and limited to Day 75 when, for male fetuses, NAD+-dependent 11B-HSD was positively correlated (r>.87; p< .06) with placental size and fetal length. These findings demonstrate the existence of porcine placental 11B-HSD activity; indicate effects of gestational age, uterine environment, and fetal sex on these activities; and suggest an association between placental 11B-HSD activity and fetal development, presumably via regulation of the amount of biologically active cortisol to which the placenta and fetus are exposed.