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Cited by 69Genetic Syndromes and ImprintingBirth, Development, and HealthPregnancy and preeclampsia studies

Developmental adaptations to increased fetal nutrient demand in mouse genetic models of Igf2‐mediated overgrowth

Angiolini, Emily, Coan, Phillip M., Sandovici, Ionel, Iwajomo, O. H., Peck, Gerrard, Burton, Graham J., Sibley, Colin P., Reik, Wolf +2 more·2011·The FASEB Journal
DOI 10.1096/fj.10-175273
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Abstract

The healthy development of the fetus depends on an optimal balance between fetal genetic drive for growth and the maternal ability to provide nutrients through the placenta. Nothing is known about fetal‐placental signaling in response to increased fetal demand in the situation of overgrowth. Here, we examined this question using the H19 Δ13 mouse model, shown previously to result in elevated levels of Igf2. Fetal and placental weights in H19 Δ13 were increased by 23% and 45%, respectively, at E19, when compared with wild‐type mice. Unexpectedly, we found that disproportionately large H19 Δ13 placentas transport 20–35% less (per gram placenta) glucose and system A amino acids and have similar reductions in passive permeability, despite a significantly greater surface area for nutrient exchange and theoretical diffusion capacity compared with wild‐type mice. Expression of key transporter genes Slc2a3 and Slc38a4 was reduced by ~20%. Decreasing the overgrowth of the H19 Δ13 placenta by genetically reducing levels of IgβPO resulted in up‐regulation of system A activity and maintenance of fetal overgrowth. Our results provide direct evidence that large placentas can modify their nutrient transfer capacity to regulate fetal nutrient acquisition. Our findings are indicative of fetal‐placental signaling mechanisms that limit total demand for maternal nutrients.—Angiolini, E., Coan, P. M., Sandovici, I., Iwajomo, O. H., Peck, G., Burton, G. J., Sibley, C. P., Reik, W., Fowden, A. L., Constância, M. Developmental adaptations to increased fetal nutrient demand in mouse genetic models of Igf2‐mediated overgrowth. FASEB J. 25, 1737–1745 (2011). www.fasebj.org

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Crossref · 10.1096/fj.10-175273

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  • There is evidence for inter-sibling competition for nutrients between mutant and wild type fetuses within mixed litters, which affects the size of the wild type pups.

    “There is also evidence for inter-sibling competition for nutrients between mutant and wild type fetuses within mixed litters, which affects the size of the wild type pups (14, 104, 124).”

    From Placental Origins of Chronic Disease (2016) · cites this paper as [14]

  • The reduced passive permeability, nutrient transport and/or transporter expression of these mutant placentas may reflect the dominance of maternal signals that constrain maternal-fetal resource allocation in the face of the increased drain posed by the overgrown conceptuses in late gestation.

    “The reduced passive permeability, nutrient transport and/or transporter expression of these mutant placentas may reflect the dominance of maternal signals that constrain maternal-fetal resource allocation in the face of the increased drain posed by the overgrown conceptuses in late gestation (14,15).”

    From Placental Origins of Chronic Disease (2016) · cites this paper as [14]

  • In the large H19-/+ mutant placenta, restriction of its transport capacity by simultaneous deletion of the Igf2P0 transcript leads to upregulation of MeAIB transport and Slc38a4 expression to meet the larger demand of the overgrown mutant fetus, with increased Igf2 expression in all its other tissues.

    “Even in the large H19 -/+ mutant placenta, restriction of its transport capacity by simultaneous deletion of the Igf2P0 transcript leads to upregulation of MeAIB transport and Slc38a4 expression to meet the larger demand of the overgrown mutant fetus, with increased Igf2 expression in all its other tissues (14).”

    From Placental Origins of Chronic Disease (2016) · cites this paper as [14]

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Authors
Angiolini, E., Coan, P. M., Sandovici, I., Iwajomo, O. H., Peck, G., Burton, G. J., Sibley, C. P., Reik, W., Fowden, A. L., & Constância, M.
Affiliations
  • Babraham Institute (GB)
  • Centre for Trophoblast Research Department of Physiology, Development, and Neuroscience University of Cambridge Cambridge UK
  • University of Cambridge (GB)
  • Manchester Academic Health Science Centre (GB)
Corresponding author
Constância, Miguel
ORCID
Venue
The FASEB Journal
Publisher
Wiley
Published
2011-01-31
Volume
25
Issue
5
Pages
1737-1745
ISSN
  • 0892-6638 (ISSN-L)
  • 1530-6860
DOI
10.1096/fj.10-175273
OpenAlex
W2116900373
Cited by
64
References
35
Citations by year
2026: 2 · 2024: 3 · 2022: 2 · 2021: 6 · 2019: 9 · 2018: 3 · 2017: 5 · 2016: 9 · 2015: 3 · 2014: 4 · 2013: 5 · 2012: 10
FWCI
4.39
Type
journal article
Language
en
Open access
closed
Licence
onlinelibrary.wiley.com/termsAndConditions#vor (vor)
Locations
  • The FASEB Journal (publishedVersion)
  • PubMed (publishedVersion)
  • Research Explorer (The University of Manchester) (submittedVersion)
Funders
Biotechnology and Biological Sciences Research Council
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Genetic Syndromes and Imprinting
  • Health Sciences › Medicine › Pediatrics, Perinatology and Child Health › Birth, Development, and Health
  • Health Sciences › Medicine › Obstetrics and Gynecology › Pregnancy and preeclampsia studies
Keywords
fetal overgrowth, insulin-like growth factor II, placental nutrient transport, glucose transport, system A amino acid transport, GLUT3, SLC38A4, placental weight, fetal growth
MeSH terms
Animals, Female, Fetus, Genotype, Insulin-Like Growth Factor II, Mice, Inbred C57BL, Mice, Mutant Strains, Placenta, Pregnancy, Mice, Knockout, RNA, Untranslated, Fetal Development, Mice, RNA, Long Noncoding

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