Adaptations in placental phenotype support fetal growth during undernutrition of pregnant mice: Undernutrition and placental phenotype
Open accessAbstract
Undernutrition during pregnancy reduces birth weight and programmes adult phenotype with consequences for life expectancy, but its effects on the phenotype of the placenta, responsible for supplying nutrients for fetal growth, remain largely unknown. Using molecular, morphological and functional analyses, placental phenotype was examined in mice during restriction of dietary intake to 80% of control from day 3 of pregnancy. At day 16, undernutrition reduced placental, but not fetal, weight in association with decreased junctional zone volume and placental expression of glucose transporter Slc2a1. At day 19, both placental and fetal weights were reduced in undernourished mice (91% and 87% of control, respectively, P < 0.01), as were the volume and surface area of the labyrinthine zone responsible for placental nutrient transfer (85% and 86%, respectively, P < 0.03). However, unidirectional materno-fetal clearance of tracer glucose was maintained and methyl-aminoisobutyric acid increased 166% (P < 0.005) per gram of undernourished placenta, relative to controls. This was associated with an 18% and 27% increased placental expression of glucose and system A amino acid transporters Slc2a1 and Slc38a2, respectively, at day 19 (P < 0.04). At both ages, undernutrition decreased expression of the placental specific transcript of the Igf2 gene by 35% (P < 0.01), although methylation of its promoter was unaffected. The placenta, therefore, adapts to help maintain fetal growth when its own growth is compromised by maternal undernutrition. Consequently, placental phenotype is responsive to environmental conditions and may help predict the risk of adult disease programmed in utero.
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Maintenance on a low protein diet throughout pregnancy results in reduced placental and pup weights, indicating that growth of the conceptus is ultimately constrained by the impoverished nutrient supply.
“However, maintenance on such a diet throughout pregnancy results in reduced placental and pup weights, indicating that growth of the conceptus is ultimately constrained by the impoverished nutrient supply (120).”
From Placental Origins of Chronic Disease (2016) · cites this paper as [120]
A 20% reduction in food intake for most of mouse pregnancy up-regulates amino acid transport per gram of placenta in association with relatively small reductions in fetal-placental weight close to term.
“For example, a 50% reduction in food intake for the second half of mouse pregnancy leads to reduced placental glucose and amino acid delivery and severe feto-placental growth restriction, whereas a 20% reduction in food intake for most of pregnancy up-regulates amino acid transport per gram of placenta in association with relatively small reductions in fetal-placental weight close to term (120, 20”
From Placental Origins of Chronic Disease (2016) · cites this paper as [120]
A 50% reduction in food intake for the second half of mouse pregnancy leads to reduced placental glucose and amino acid delivery and severe feto-placental growth restriction.
“For example, a 50% reduction in food intake for the second half of mouse pregnancy leads to reduced placental glucose and amino acid delivery and severe feto-placental growth restriction, whereas a 20% reduction in food intake for most of pregnancy up-regulates amino acid transport per gram of placenta in association with relatively small reductions in fetal-placental weight close to term (120, 20”
From Placental Origins of Chronic Disease (2016) · cites this paper as [120]
Changes in placental Igf2P0 expression occur in response to maternal undernutrition and feeding an obesogenic diet, so this gene transcript may have an important role in adapting placental phenotype to environmental cues.
“Since changes in placental Igf2P0 expression occur in response to maternal undernutrition and feeding an obesogenic diet (120, 496), this gene transcript may have an important role in adapting placental phenotype to environmental cues.”
From Placental Origins of Chronic Disease (2016) · cites this paper as [120]
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- Sferruzzi-Perri AN, Coan PM, Vaughan OR, Constancia M, Burton GJ, Fowden AL. Igf2 deficiency modifies placental adaptation to maternal undernutrition. Reprod Sci. 2009;16:165A. [Google Scholar]
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- Authors
- Coan, P. M., Vaughan, O. R., Sekita, Y., Finn, S. L., Burton, G. J., Constancia, M., & Fowden, A. L.
- Affiliations
- University of Cambridge (GB)
- Corresponding author
- Coan, P. M.
- Venue
- The Journal of Physiology
- Publisher
- Wiley
- Published
- 2010-01-29
- Volume
- 588
- Issue
- 3
- Pages
- 527-538
- ISSN
- 0022-3751 (ISSN-L)
- PMC
- PMC2825615
- OpenAlex
- W2156185929
- Cited by
- 199
- References
- 53
- Citations by year
- 2026: 4 · 2025: 5 · 2024: 6 · 2023: 7 · 2022: 11 · 2021: 13 · 2020: 12 · 2019: 8 · 2018: 18 · 2017: 11 · 2016: 11 · 2015: 22 · 2014: 10 · 2013: 11 · 2012: 24
- FWCI
- 14.53
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- The Journal of Physiology (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- UCL Discovery (University College London) (submittedVersion)
- Research Explorer (The University of Manchester) (submittedVersion)
- Funders
- Biotechnology and Biological Sciences Research Council (BB/B50118X/1, BB/C513626/1, BB/B50118X/2)
- Topics
- Health Sciences › Medicine › Pediatrics, Perinatology and Child Health › Birth, Development, and Health
- Health Sciences › Medicine › Obstetrics and Gynecology › Pregnancy and preeclampsia studies
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Genetic Syndromes and Imprinting
- Keywords
- maternal undernutrition, fetal growth, placental nutrient transfer, amino acid transporters, insulin-like growth factor II, methionine restriction, labyrinth zone, junctional zone, fetal programming, birth weight
- MeSH terms
- Adaptation, Physiological, Animals, Diet, Female, Insulin-Like Growth Factor II, Mice, Inbred C57BL, Phenotype, Placenta, Placentation, Pregnancy, Models, Animal, Amino Acid Transport System A, Maternal Nutritional Physiological Phenomena, Malnutrition, Fetal Development, Glucose Transporter Type 1, Mice
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