Journal
BEST PRACTICE & RESEARCH CLINICAL ENDOCRINOLOGY & METABOLISM
Volume 26, Issue 5, Pages 689-700Publisher
ELSEVIER SCI LTD
DOI: 10.1016/j.beem.2012.03.007
Keywords
glucocorticoids; programming; 11 beta-hydroxysteroid dehydrogenase; hypothalamic-pituitary-adrenal axis; epigenetic
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Funding
- Chief Scientist Office [SCD/09] Funding Source: researchfish
- Medical Research Council [G0501904] Funding Source: researchfish
- Medical Research Council [G0501904] Funding Source: Medline
- Chief Scientist Office [SCD/09] Funding Source: Medline
- MRC [G0501904] Funding Source: UKRI
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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. (C) 2012 Elsevier Ltd. All rights reserved.
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