Journalartikel

Rhythm of Fetoplacental 11β-Hydroxysteroid Dehydrogenase Type 2-Fetal Protection From Morning Maternal Glucocorticoids


AutorenlisteLamade, Eva Kathrin; Hendlmeier, Ferdinand; Wudy, Stefan A.; Witt, Stephanie H.; Rietschel, Marcella; Coenen, Michaela; Gilles, Maria; Deuschle, Michael

Jahr der Veröffentlichung2021

Seiten1630-1636

ZeitschriftThe Journal of Clinical Endocrinology & Metabolism

Bandnummer106

Heftnummer6

ISSN0021-972X

eISSN1945-7197

Open Access StatusBronze

DOI Linkhttps://doi.org/10.1210/clinem/dgab113

VerlagOxford University Press


Abstract

Context: Excess glucocorticoids impact fetal health. Maternal glucocorticoids peak in early morning. Fetoplacental 11 beta-hydroxysteroid dehydrogenase type 2 (11 beta-HSD2) inactivates cortisol to cortisone, protecting the fetus from high glucocorticoids. However, time-specific alterations of human fetoplacental 11 beta-HSD2 have not been studied.

Objective: We hypothesized that fetoplacental 11 beta-HSD2 activity shows time-specific alteration and acute affective or anxiety disorders impact fetoplacental 11 beta-HSD2 activity.

Methods: In this observational study we investigated 78 pregnant European women undergoing amniocentesis (15.9 +/- 0.9 weeks of gestation). Amniotic fluid was collected (8:00 to 16:30 hours) for analysis of fetoplacental 11 beta-HSD2 activity, using cortisol (F):cortisone (E) ratio in amniotic fluid, E/(E + F). Fetoplacental 11 beta-HSD2 rhythm and association with "acute affective or anxiety disorder" (patients with at least one of: a major depressive episode, specific phobia, panic disorder, generalized anxiety disorder, mixed anxiety and depressive disorder) and "acute anxiety disorder" (one of: panic disorder, generalized anxiety disorder, mixed anxiety, depressive disorder), assessed using Mini International Neuropsychiatric Interview, were investigated.

Results: Activity of 11 beta-HSD2 correlated with time of amniocentesis, peaking in the morning (r = -0.398; P < 0.001) and increased with acute affective or anxiety disorder (mean [M] = 0.70 vs M = 0.74; P = 0.037) and acute anxiety disorder (M = 0.70 vs M = 0.75; P = 0.016). These associations remained significant when controlling for confounders. 11 beta-HSD2 activity correlated negatively with pre-pregnancy body mass index (r = -0.225; P = 0.047).

Conclusion: Our study indicates a time-specific alteration of fetoplacental 11 beta-HSD2 activity with peaking levels in the morning, demonstrating a mechanism of fetal protection from the morning maternal glucocorticoid surge.




Zitierstile

Harvard-ZitierstilLamade, E., Hendlmeier, F., Wudy, S., Witt, S., Rietschel, M., Coenen, M., et al. (2021) Rhythm of Fetoplacental 11β-Hydroxysteroid Dehydrogenase Type 2-Fetal Protection From Morning Maternal Glucocorticoids, The Journal of Clinical Endocrinology & Metabolism, 106(6), pp. 1630-1636. https://doi.org/10.1210/clinem/dgab113

APA-ZitierstilLamade, E., Hendlmeier, F., Wudy, S., Witt, S., Rietschel, M., Coenen, M., Gilles, M., & Deuschle, M. (2021). Rhythm of Fetoplacental 11β-Hydroxysteroid Dehydrogenase Type 2-Fetal Protection From Morning Maternal Glucocorticoids. The Journal of Clinical Endocrinology & Metabolism. 106(6), 1630-1636. https://doi.org/10.1210/clinem/dgab113



Schlagwörter


11 beta-hydroxysteroid dehydrogenaseAMNIOTIC-FLUID GLUCOCORTICOIDScircadianCLOCK GENESCORTISOL STRESS REACTIVITYFETALfetoplacentalPLACENTAL 11-BETA-HSD2


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