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Related Experiment Videos

Glucocorticoids, 11beta-hydroxysteroid dehydrogenase, and fetal programming.

J R Seckl1, M Cleasby, M J Nyirenda

  • 1Molecular Medicine Center, University of Edinburgh, Western General Hospital, Edinburgh, Scotland, United Kingdom. J.Seckl@ed.ac.uk

Kidney International
|April 12, 2000
PubMed
Summary

Fetal exposure to glucocorticoids, or stress hormones, can program babies for adult diseases like hypertension and diabetes. This programming involves lasting changes in gene expression, potentially explaining links between early life and later health.

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Area of Science:

  • Endocrinology
  • Developmental Biology
  • Public Health

Background:

  • Low birth weight is linked to increased adult cardiovascular and metabolic disease risk.
  • Fetal programming suggests early life events impact later health.
  • Prenatal glucocorticoid exposure can reduce birth weight and cause long-term effects.

Purpose of the Study:

  • To investigate if fetal overexposure to endogenous glucocorticoids links early life events to adult disease.
  • To explore the role of 11beta-hydroxysteroid dehydrogenase type 2 (11beta-HSD2) in glucocorticoid programming.

Main Methods:

  • Administered dexamethasone or carbenoxolone to pregnant rats to alter glucocorticoid exposure.
  • Measured birth weight, adult blood pressure, glucose levels, and hypothalamic-pituitary-adrenal (HPA) axis activity in offspring.

Related Experiment Videos

  • Examined placental 11beta-HSD2 activity and its correlation with fetal weight.
  • Reviewed human studies on 11beta-HSD2 gene mutations, placental activity, and adult cortisol levels.

    • Main Results:

    • Prenatal glucocorticoid exposure in rats reduced birth weight, leading to adult hypertension, hyperglycemia, and increased HPA axis activity.
    • Placental 11beta-HSD2 activity correlated with fetal weight.
    • Human studies show 11beta-HSD2 gene mutations cause low birth weight and reduced placental activity is linked to intrauterine growth restriction.
    • Low birth weight humans exhibit higher adult cortisol levels, indicating HPA axis programming.

    Conclusions:

    • Fetal overexposure to glucocorticoids, potentially due to reduced placental 11beta-HSD2 activity, can program offspring for adult metabolic and cardiovascular diseases.
    • Glucocorticoid programming involves permanent, tissue-specific changes in gene expression, including the glucocorticoid receptor.
    • This mechanism offers a partial explanation for the association between fetal development and later-life disease risk.