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Fetal programming of cardiovascular function through exposure to maternal undernutrition
Open accessAbstract
A substantial and robust body of epidemiological evidence indicates that prenatal dietary experience may be a factor determining cardiovascular disease risk. Retrospective cohort studies indicate that low birth weight and disproportion at birth are powerful predictors of later disease risk. This prenatal influence on non-communicable disease in later life has been termed programming. Maternal nutritional status has been proposed to be the major programming influence on the developing fetus. The evidence from epidemiological studies of nutrition, fetal development and birth outcome is, however, often weak and inconclusive. The validity of the nutritional programming concept is highly dependent on experimental studies in animals. The feeding of low-protein diets in rat pregnancy results in perturbations in fetal growth and dimensions at birth. The offspring of rats fed low-protein diets exhibit a number of metabolic and physiological disturbances, and are consistently found to have high blood pressure from early postnatal life. This experimental model has been used to explore potential mechanisms of programming through which maternal diet may programme the cardiovascular function of the fetus. Indications from this work are that fetal exposure to maternally-derived glucocorticoids plays a key role in the programming mechanism. Secondary to this activity, the fetal hypothalamic–pituitary–adrenal axis may stimulate renin–angiotensin system activity, resulting in increased vascular resistance and hypertension.
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“Individuals whose gestation coincided with the famine exhibited increased susceptibility to obesity, insulin resistance, and cardiovascular disease in adulthood, strongly implicating fetal adaptive responses to nutrient scarcity in shaping lifelong disease risk [10,11].”
From Maternal Overnutrition and Fetal Programming: Long-Term Metabolic, Cognitive, and Epigenetic Consequences (2026) · cites this paper as [10]
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Metadata
- Authors
- Langley-Evans, S. C.
- Venue
- Proceedings of the Nutrition Society
- Publisher
- Cambridge University Press (CUP)
- Published
- 2001-11
- Volume
- 60
- Issue
- 4
- Pages
- 505-513
- ISSN
- 0029-6651 (ISSN-L)
- 1475-2719
- OpenAlex
- W2135897417
- Cited by
- 203
- References
- 94
- Citations by year
- 2026: 2 · 2025: 1 · 2024: 4 · 2023: 5 · 2022: 3 · 2021: 2 · 2020: 4 · 2019: 3 · 2018: 4 · 2017: 3 · 2016: 6 · 2015: 6 · 2014: 15 · 2013: 9 · 2012: 6
- FWCI
- 2.22
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Proceedings of The Nutrition Society (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Health Sciences › Medicine › Pediatrics, Perinatology and Child Health › Birth, Development, and Health
- Health Sciences › Medicine › Obstetrics and Gynecology › Pregnancy and preeclampsia studies
- Health Sciences › Medicine › Pediatrics, Perinatology and Child Health › Prenatal Substance Exposure Effects
- Keywords
- fetal programming, maternal undernutrition, cardiovascular risk, low birth weight, fetal growth restriction, prenatal nutrition, low-protein diet, hypertension, glucocorticoids, hypothalamic-pituitary-adrenal axis, renin-angiotensin system, vascular resistance
- MeSH terms
- Animals, Birth Weight, Cardiovascular Diseases, Disease Models, Animal, Female, Glucocorticoids, Humans, Hypertension, Kidney, Nutrition Disorders, Pregnancy, Pregnancy Complications, Prenatal Exposure Delayed Effects, Renin-Angiotensin System, Risk Factors, Rats
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Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
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