Glucocorticoids as mediators of developmental programming effects

Khulan Batbayar, Amanda J. Drake

Research output: Contribution to journalReview article

58 Citations (Scopus)

Abstract

Epidemiological evidence suggests that exposure to an adverse environment in early life is associated with an increased risk of cardio-metabolic and behavioral disorders in adulthood, a phenomenon termed 'early life programming'. One major hypothesis for early life programming is fetal glucocorticoid overexposure. In animal studies, prenatal glucocorticoid excess as a consequence of maternal stress or through exogenous administration to the mother or fetus is associated with programming effects on cardiovascular and metabolic systems and on the brain. These effects can be transmitted to subsequent generations. Studies in humans provide some evidence that prenatal glucocorticoid exposure may exert similar programming effects on glucose/insulin homeostasis, blood pressure and neurodevelopment. The mechanisms by which glucocorticoids mediate these effects are unclear but may include a role for epigenetic modifications. This review discusses the evidence for glucocorticoid programming in animal models and in humans.

Original languageEnglish (US)
Pages (from-to)689-700
Number of pages12
JournalBest Practice and Research: Clinical Endocrinology and Metabolism
Volume26
Issue number5
DOIs
StatePublished - Oct 1 2012
Externally publishedYes

Fingerprint

Glucocorticoids
Fetal Development
Cardiovascular System
Epigenomics
Fetus
Homeostasis
Animal Models
Mothers
Insulin
Blood Pressure
Glucose
Brain

Keywords

  • 11β-hydroxysteroid dehydrogenase
  • epigenetic
  • glucocorticoids
  • hypothalamic-pituitary-adrenal axis
  • programming

ASJC Scopus subject areas

  • Endocrinology
  • Endocrinology, Diabetes and Metabolism

Cite this

Glucocorticoids as mediators of developmental programming effects. / Batbayar, Khulan; Drake, Amanda J.

In: Best Practice and Research: Clinical Endocrinology and Metabolism, Vol. 26, No. 5, 01.10.2012, p. 689-700.

Research output: Contribution to journalReview article

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