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Foetal and placental 11β-HSD2: a hub for developmental programming.
E C Cottrell1, J R Seckl, M C Holmes
1Maternal and Fetal Health Research Centre, Institute of Human Development, University of Manchester, Manchester, UK.
Acta Physiologica (Oxford, England)
|December 17, 2013
Summary
Foetal growth restriction is linked to excess prenatal glucocorticoid exposure, regulated by 11β-hydroxysteroid dehydrogenase type 2 (11β-HSD2). This enzyme’s placental deficiency impairs foetal growth and programs adult disease risk.
Area of Science:
- Developmental biology
- Endocrinology
- Perinatal medicine
Background:
- Foetal growth restriction (FGR) increases perinatal mortality and adult disease risk.
- Excess prenatal glucocorticoid exposure is a key mechanism underlying FGR.
- The enzyme 11β-hydroxysteroid dehydrogenase type 2 (11β-HSD2) regulates foetal glucocorticoid exposure.
Purpose of the Study:
- To investigate the direct significance of 11β-HSD2 for developmental programming.
- To examine the role of feto-placental 11β-HSD2 in placental function, neurodevelopment, and adult behavior.
Main Methods:
- Utilized a mouse knockout model lacking 11β-HSD2.
- Investigated placental function, neurodevelopment, and adult behavior in the knockout model.
Main Results:
- Down-regulation or deficiency of placental 11β-HSD2 is associated with reduced foetal growth and birth weight.
- Evidence from the mouse model highlights a critical role for feto-placental 11β-HSD2 in adverse programming outcomes.
- 11β-HSD2 deficiency impacts neurodevelopment and adult behavior.
Conclusions:
- Feto-placental 11β-HSD2 is crucial for preventing adverse developmental programming.
- Understanding 11β-HSD2 function is vital for mitigating FGR and its long-term consequences.
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