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Cited by 536Pregnancy and preeclampsia studiesBirth, Development, and HealthAdrenal Hormones and Disorders

The DOI matches its Crossref record.

Placental 11β‐hydroxysteroid dehydrogenase: a key regulator of fetal glucocorticoid exposure

Benediktsson, Rafn, Calder, Andrew A., Edwards, Christopher R. W., Seckl, Jonathan R.·1997·Clinical Endocrinology
DOI 10.1046/j.1365-2265.1997.1230939.x
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Abstract

OBJECTIVE: Placental 11 beta-hydroxysteroid dehydrogenase (11 beta-HSD), which converts active cortisol to inactive cortisone, has been proposed to be the mechanism guarding the fetus from the growth retarding effects of maternal glucocorticoids; however, other placental enzymes have also been implicated. Placental 11 beta-HSD is unstable in vitro, and enzyme activity thus detected may not be relevant to the proposed barrier role. We have therefore examined placental glucocorticoid metabolism in dually perfused freshly isolated intact human placentas. DESIGN: Placentas were obtained from randomly selected normal term deliveries. The maternal circuit was perfused with physiological concentration of cortisol, the fetal effluent collected and steroid metabolites separated and quantified using silica columns (Sep-pak Plus) and HPLC. RESULTS: Most of the maternally administered cortisol was metabolized to cortisone, and no conversion of cortisone to cortisol was detected. Cortisone was the only product of cortisol metabolism. Inhibition of 11 beta-HSD with glycyrrhetinic acid allowed cortisol to gain direct access to the fetal circulation. CONCLUSION: We conclude that human placental 11 beta-HSD plays a crucial role in controlling glucocorticoid access to the fetus. Other enzymes are not significant contributors at physiologically relevant cortisol concentrations.

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Metadata

Authors
Benediktsson, R., Calder, A. A., Edwards, C. R. W., & Seckl, J. R.
Affiliations
  • Western General Hospital (GB)
  • University of Edinburgh (GB)
ORCID
Venue
Clinical Endocrinology
Publisher
Wiley
Published
1997-02
Volume
46
Issue
2
Pages
161-166
ISSN
  • 0300-0664 (ISSN-L)
  • 1365-2265
DOI
10.1046/j.1365-2265.1997.1230939.x
OpenAlex
W2020469940
Cited by
536
References
0
Citations by year
2026: 10 · 2025: 12 · 2024: 14 · 2023: 20 · 2022: 18 · 2021: 18 · 2020: 20 · 2019: 27 · 2018: 22 · 2017: 29 · 2016: 36 · 2015: 31 · 2014: 31 · 2013: 26 · 2012: 37
FWCI
12.08
Type
journal article
Language
en
Open access
closed
Licence
onlinelibrary.wiley.com/termsAndConditions#vor (vor, 2461 d)
Locations
  • Clinical Endocrinology (publishedVersion)
  • PubMed (publishedVersion)
Funders
Wellcome Trust
Topics
  • Health Sciences › Medicine › Obstetrics and Gynecology › Pregnancy and preeclampsia studies
  • Health Sciences › Medicine › Pediatrics, Perinatology and Child Health › Birth, Development, and Health
  • Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Adrenal Hormones and Disorders
Keywords
fetal glucocorticoid exposure, cortisol metabolism, cortisone, human placenta, glycyrrhetinic acid, fetal growth
MeSH terms
Administration, Topical, Anti-Inflammatory Agents, Cortisone, Female, Glycyrrhetinic Acid, Humans, Hydrocortisone, Hydroxysteroid Dehydrogenases, Organ Culture Techniques, Perfusion, Placenta, 11-beta-Hydroxysteroid Dehydrogenases

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