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Related Experiment Videos

Glucocorticoid programming.

Jonathan R Seckl1, Michael J Meaney

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

Annals of the New York Academy of Sciences
|January 29, 2005
PubMed
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Adverse fetal environments, particularly excess prenatal glucocorticoids, permanently program adult health, increasing risks for cardiovascular and metabolic disorders. This programming involves changes in the glucocorticoid receptor, affecting long-term health outcomes.

Area of Science:

  • Endocrinology
  • Developmental Biology
  • Neuroendocrinology

Background:

  • Adverse fetal environments are linked to adult chronic diseases.
  • Prenatal glucocorticoid exposure may mediate this link, impacting fetal development and adult pathophysiology.
  • The enzyme 11beta-hydroxysteroid dehydrogenase type 2 (11beta-HSD2) acts as a protective barrier against maternal glucocorticoids.

Purpose of the Study:

  • To investigate the long-term physiological and molecular consequences of prenatal glucocorticoid exposure.
  • To explore the role of 11beta-HSD2 in mediating the effects of prenatal glucocorticoids.
  • To understand the mechanisms underlying fetal programming of adult diseases.

Main Methods:

  • Animal models were used to study the effects of prenatal glucocorticoid exposure or 11beta-HSD2 inhibition.

Related Experiment Videos

  • Human studies examined 11beta-HSD2 gene mutations and their association with birth weight and intrauterine growth retardation.
  • Molecular analyses focused on changes in glucocorticoid receptor gene expression and transcription factors.

    • Main Results:

    • Prenatal glucocorticoid excess or reduced 11beta-HSD2 activity in animal models led to low birth weight, hypertension, hyperglycemia, and altered hypothalamic-pituitary-adrenal (HPA) axis activity.
    • In humans, 11beta-HSD2 mutations and reduced placental activity were linked to low birth weight and intrauterine growth retardation.
    • Low birth weight individuals exhibited higher adult plasma cortisol levels, suggesting HPA axis programming.
    • Molecular findings indicated permanent alterations in glucocorticoid receptor gene expression.

    Conclusions:

    • Prenatal exposure to excess glucocorticoids, or impaired placental protection by 11beta-HSD2, permanently programs adult physiology.
    • This programming increases susceptibility to cardiovascular, metabolic, and neuroendocrine disorders.
    • Alterations in glucocorticoid receptor expression are key molecular mechanisms underlying these long-term effects.