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Fetal osteocalcin levels are related to placental 11 beta-hydroxysteroid dehydrogenase activity in humans
R Benediktsson1, J Brennand, L Tibi
1University Department of Medicine, Western General Hospital, Scotland, UK.
Insights
Cord blood osteocalcin levels indicate how well the placenta inactivates maternal glucocorticoids. This finding suggests osteocalcin may predict hypertension risk in newborns.
Area of Science:
- Endocrinology
- Reproductive Biology
- Perinatal Medicine
Background:
- In utero glucocorticoid overexposure can lead to reduced birth weight and offspring hypertension.
- Placental 11 beta-hydroxysteroid dehydrogenase (11 beta-HSD) protects the fetus by converting cortisol to cortisone.
- Osteocalcin in adult blood is a known marker for glucocorticoid exposure.
Purpose of the Study:
- To investigate the relationship between cord blood osteocalcin levels and placental 11 beta-HSD activity.
- To determine if osteocalcin can serve as a marker for fetal exposure to glucocorticoids.
Main Methods:
- A cross-sectional study was conducted with 21 women at delivery.
- Cord blood samples were analyzed for osteocalcin, cortisol, and cortisone via radioimmunoassay.
- Placental 11 beta-HSD activity was assessed using calculated indices.
Main Results:
- A significant positive correlation was observed between placental 11 beta-HSD activity indices and cord blood osteocalcin levels.
- The placental 11 beta-HSD Activity Index directly correlated with osteocalcin (Pearson's r = +0.58, P < 0.02).
Conclusions:
- Term cord blood osteocalcin levels reflect the efficiency of placental glucocorticoid inactivation.
- Osteocalcin may serve as a potential biomarker for predicting the risk of adult hypertension in offspring.
Objective:
Overexposure to glucocorticoids in utero reduces birth weight and, in animals, leads to persistent hypertension in the offspring. The fetus is normally protected from maternal glucocorticoids by placental 11 beta-hydroxysteroid dehydrogenase (11 beta-HSD) which catalyses the conversion of cortisol to inert cortisone. In adult humans, osteocalcin is a sensitive marker of glucocorticoid exposure. The aim of this study was to determine whether cord blood osteocalcin levels were related to the ability of placental 11 beta-HSD to inactivate maternal cortisol.
Design:
Cross-sectional study examining the relation between cord blood levels of osteocalcin and placental glucocorticoid metabolism at term.
Patients:
Twenty-one women attending for delivery at the Simpson Memorial Maternity Pavilion in Edinburgh had cord venous and arterial blood samples collected at delivery.
Measurements:
Cord plasma levels of osteocalcin, cortisol and cortisone were measured by radioimmunoassay and indices of placental 11 beta-HSD activity were calculated.
Results:
All indices of placental 11 beta-hydroxysteroid dehydrogenase activity correlated directly and significantly with cord blood osteocalcin levels. For cord blood osteocalcin and the placental 11 beta-HSD Activity Index, Pearson's r was +0.58, r2 = 0.33 and P < 0.02.
Conclusion:
We conclude that term cord blood osteocalcin level reflects the effectiveness of placental glucocorticoid inactivation, and may be a marker for the development of adult hypertension.