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Prenatal glucocorticoids and long-term programming

Jonathan R Seckl1

  • 1Endocrinology Unit, University of Edinburgh, Western General Hospital, Edinburgh EH4 2XU, UK. J.Seckl@ed.ac.uk

European Journal of Endocrinology
|November 24, 2004
PubMed

Insights

Prenatal exposure to excess glucocorticoids or stress in rats programs adult-onset cardiovascular, metabolic, and neuroendocrine disorders. This prenatal programming is linked to low birth weight and altered glucocorticoid receptor (GR) gene expression.

Area of Science:

  • Endocrinology
  • Developmental Biology
  • Physiology

Background:

  • Low birth weight is linked to adult cardiovascular, metabolic, and neuroendocrine disorders.
  • Glucocorticoids administered during pregnancy reduce birth weight and affect organ maturation.
  • Prenatal glucocorticoid or stress exposure may link fetal growth to adult pathophysiology.

Purpose of the Study:

  • To investigate if prenatal exposure to excess glucocorticoids or stress programs adult pathophysiology.
  • To explore the role of 11beta-hydroxysteroid dehydrogenase type 2 (11beta-HSD2) in this process.

Main Methods:

  • Administered dexamethasone or carbenoxolone to pregnant rats to reduce fetal weight.
  • Assessed adult offspring for hypertension, hyperglycemia, hypothalamic-pituitary-adrenal (HPA) axis activity, and anxiety-like behavior.
  • Correlated placental 11beta-HSD2 activity with fetal weight.
  • Examined glucocorticoid receptor (GR) gene expression in adult offspring.

Main Results:

  • Prenatal dexamethasone or carbenoxolone exposure resulted in low birth weight offspring.
  • Adult offspring exhibited hypertension, hyperglycemia, increased HPA axis activity, and anxiety-like behaviors.
  • Placental 11beta-HSD2 activity positively correlated with fetal weight.
  • Low birth weight in humans is associated with higher adult cortisol levels and HPA axis programming.
  • Evidence suggests permanent changes in GR gene expression contribute to programming.

Conclusions:

  • Prenatal exposure to excess glucocorticoids, either pharmacologically or physiologically, programs adult cardiovascular, metabolic, and neuroendocrine disorders.
  • The placental enzyme 11beta-HSD2 plays a crucial role in protecting the fetus from maternal glucocorticoids.
  • Altered glucocorticoid receptor (GR) programming is a potential molecular mechanism underlying these long-term effects.

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