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The Mother or the Fetus? 11β-Hydroxysteroid Dehydrogenase Type 2 Null Mice Provide Evidence for Direct Fetal Programming of Behavior by Endogenous Glucocorticoids
Open accessAbstract
Low birth weight associates with increased susceptibility to adult cardiometabolic and affective disorders spawning the notion of fetal “programming.” Prenatal exposure to excess glucocorticoids may be causal. In support, maternal stress or treatment during pregnancy with dexamethasone (which crosses the placenta) or inhibitors of fetoplacental 11β-hydroxysteroid dehydrogenase type 2 (11β-HSD2), the physiological “barrier” to maternal glucocorticoids, reduces birth weight and programs permanent offspring hypertension, hyperglycemia, and anxiety behaviors. It remains uncertain whether such effects are mediated indirectly via altered maternal function or directly on the fetus and its placenta. To dissect this critical issue, we mated 11β-HSD2 +/− mice such that each pregnant female produces +/+, +/−, and −/− offspring and compared them with offspring of homozygous wild-type and −/− matings. We show that 11β-HSD2 −/− offspring of either +/− or −/− mothers have lower birth weight and exhibit greater anxiety than 11β-HSD2 +/+ littermates. This provides clear evidence for the key role of fetoplacental 11β-HSD2 in prenatal glucocorticoid programming.
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“In addition, deletion of the 11-ßHSD2 gene in mice is associated with fetal growth restriction (261).”
From Placental Origins of Chronic Disease (2016) · cites this paper as [261]
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11β-HSD1, Inflammation, Metabolic Disease and Age-related Cognitive (dys)Function
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Alterations of Cortisol Metabolism in Human Disorders
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The Effects of Glucocorticoids on Fetal and Placental Development
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Metadata
- Authors
- Holmes, M. C., Abrahamsen, C. T., French, K. L., Paterson, J. M., Mullins, J. J., & Seckl, J. R.
- Affiliations
- The Queen's Medical Research Institute (GB)
- Venue
- The Journal of Neuroscience
- Publisher
- Society for Neuroscience
- Published
- 2006-04-05
- Volume
- 26
- Issue
- 14
- Pages
- 3840-3844
- ISSN
- 0270-6474 (ISSN-L)
- 1529-2401
- PMC
- PMC6445356
- OpenAlex
- W1971789895
- Cited by
- 200
- References
- 33
- Citations by year
- 2026: 5 · 2025: 1 · 2024: 2 · 2023: 9 · 2022: 4 · 2021: 6 · 2020: 10 · 2019: 8 · 2018: 3 · 2017: 10 · 2016: 16 · 2015: 21 · 2014: 22 · 2013: 9 · 2012: 18
- FWCI
- 10.85
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Licence
- Locations
- Journal of Neuroscience (publishedVersion, cc-by-nc-sa)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Edinburgh Research Explorer (University of Edinburgh) (submittedVersion, other-oa)
- Funders
- Wellcome Trust (079009)
- Medical Research Council
- Topics
- Health Sciences › Medicine › Pediatrics, Perinatology and Child Health › Birth, Development, and Health
- Life Sciences › Neuroscience › Behavioral Neuroscience › Stress Responses and Cortisol
- Health Sciences › Medicine › Pediatrics, Perinatology and Child Health › Prenatal Substance Exposure Effects
- Keywords
- 11β-hydroxysteroid dehydrogenase type 2, fetal programming, antenatal glucocorticoids, anxiety-like behavior, birth weight, placenta, dexamethasone, maternal stress, low birth weight, offspring behavior, glucocorticoid metabolism
- MeSH terms
- Animals, Anxiety, Behavior, Animal, Birth Weight, Female, Fetus, Glucocorticoids, Male, Mice, Inbred C57BL, Mothers, Placenta, Pregnancy, Mineralocorticoid Excess Syndrome, Apparent, 11-beta-Hydroxysteroid Dehydrogenase Type 2, Mice
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