Fetal programming of hypothalamo‐pituitary‐adrenal function: prenatal stress and glucocorticoids
Open accessAbstract
Prenatal stress (PS) and maternal exposure to exogenous glucocorticoids can lead to permanent modification of hypothalamo‐pituitary‐adrenal (HPA) function and stress‐related behaviour. Both of these manipulations lead to increased fetal exposure to glucocorticoids. Glucocorticoids are essential for many aspects of normal brain development, but exposure of the fetal brain to an excess of glucocorticoids can have life‐long effects on neuroendocrine function. Both endogenous glucocorticoid and synthetic glucocorticoid exposure have a number of rapid effects in the fetal brain, including modification of neurotransmitter systems and transcriptional machinery. Such fetal exposure permanently alters HPA function in prepubertal, postpubertal and ageing offspring, in a sex‐dependent manner. Prenatal stress and exogenous glucocorticoid manipulation also lead to the modification of behaviour, brain and organ morphology, as well as altered regulation of other endocrine systems. It is also becoming increasingly apparent that the timing of exposure to PS or synthetic glucocorticoids has tremendous effects on the nature of the phenotypic outcome. Permanent changes in endocrine function will ultimately impact on health in both human and animal populations.
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As WAT develops postnatally in some species like rats and mice, changes induced by maternal manipulations may also be the result of alterations in other systems, particularly the hypothalamic pituitary adrenal hormonal axis in the offspring during gestation.
“However, as WAT develops postnatally in some species like rats and mice, changes induced by maternal manipulations may also be the result of alterations in other systems, particularly the hypothalamic pituitary adrenal hormonal axis in the offspring during gestation [138].”
From Developmental programming of offspring adipose tissue biology and obesity risk (2021) · cites this paper as [138]
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- Authors
- Kapoor, A., Dunn, E., Kostaki, A., Andrews, M. H., & Matthews, S. G.
- Affiliations
- University of Toronto (CA)
- Corresponding author
- Matthews, Stephen G.
- Venue
- The Journal of Physiology
- Publisher
- Wiley
- Published
- 2006-03-28
- Volume
- 572
- Issue
- 1
- Pages
- 31-44
- ISSN
- 0022-3751 (ISSN-L)
- 1469-7793
- PMC
- PMC1779638
- OpenAlex
- W2121411996
- Cited by
- 598
- References
- 11
- Citations by year
- 2026: 12 · 2025: 15 · 2024: 19 · 2023: 35 · 2022: 28 · 2021: 31 · 2020: 29 · 2019: 31 · 2018: 37 · 2017: 29 · 2016: 42 · 2015: 40 · 2014: 31 · 2013: 34 · 2012: 35
- FWCI
- 2.96
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- The Journal of Physiology (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Life Sciences › Neuroscience › Behavioral Neuroscience › Stress Responses and Cortisol
- Health Sciences › Medicine › Pediatrics, Perinatology and Child Health › Birth, Development, and Health
- Health Sciences › Medicine › Public Health, Environmental and Occupational Health › Maternal Mental Health During Pregnancy and Postpartum
- Keywords
- fetal programming, hypothalamic-pituitary-adrenal axis, prenatal stress, glucocorticoids, maternal glucocorticoid exposure, stress behavior, neuroendocrine development, sex differences, exposure timing, brain structure, hormonal regulation
- MeSH terms
- Animals, Female, Glucocorticoids, Humans, Hypothalamo-Hypophyseal System, Pituitary-Adrenal System, Pregnancy, Prenatal Exposure Delayed Effects, Receptors, Glucocorticoid, Stress, Physiological, Fetal Development
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