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Glucocorticoids, prenatal stress and the programming of disease
Author(s):
Anjanette Harris
,
Jonathan Seckl
Publication date
Created:
March 2011
Publication date
(Print):
March 2011
Journal:
Hormones and Behavior
Publisher:
Elsevier BV
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PubMed
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Abstract
An adverse foetal environment is associated with increased risk of cardiovascular, metabolic, neuroendocrine and psychological disorders in adulthood. Exposure to stress and its glucocorticoid hormone mediators may underpin this association. In humans and in animal models, prenatal stress, excess exogenous glucocorticoids or inhibition of 11β-hydroxysteroid dehydrogenase type 2 (HSD2; the placental barrier to maternal glucocorticoids) reduces birth weight and causes hyperglycemia, hypertension, increased HPA axis reactivity, and increased anxiety-related behaviour. Molecular mechanisms that underlie the 'developmental programming' effects of excess glucocorticoids/prenatal stress include epigenetic changes in target gene promoters. In the case of the intracellular glucocorticoid receptor (GR), this alters tissue-specific GR expression levels, which has persistent and profound effects on glucocorticoid signalling in certain tissues (e.g. brain, liver, and adipose). Crucially, changes in gene expression persist long after the initial challenge, predisposing the individual to disease in later life. Intriguingly, the effects of a challenged pregnancy appear to be transmitted possibly to one or two subsequent generations, suggesting that these epigenetic effects persist. Copyright © 2010 Elsevier Inc. All rights reserved.
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Author and article information
Journal
Title:
Hormones and Behavior
Abbreviated Title:
Hormones and Behavior
Publisher:
Elsevier BV
ISSN (Print):
0018506X
Publication date Created:
March 2011
Publication date (Print):
March 2011
Volume
: 59
Issue
: 3
Pages
: 279-289
Article
DOI:
10.1016/j.yhbeh.2010.06.007
PubMed ID:
20591431
SO-VID:
370d7d6c-470e-431a-9ce2-2a2261f1cd7e
Copyright ©
© 2011
License:
https://www.elsevier.com/tdm/userlicense/1.0/
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