The DOI matches its Crossref record; 34 of the 34 references it cites were found in a registry or an index.
Adaptation of nutrient supply to fetal demand in the mouse involves interaction between the Igf2 gene and placental transporter systems
Open accessAbstract
The mammalian fetus is unique in its dependence during gestation on the supply of maternal nutrients through the placenta. Maternal supply and fetal demand for nutrients need to be fine tuned for healthy growth and development of the fetus along its genetic trajectory. An altered balance between supply and demand can lead to deviations from this trajectory with long-term consequences for health. We have previously shown that in a knockout lacking the imprinted placental-specific Igf2 transcript (P0), growth of the placenta is compromised from early gestation but fetal growth is normal until late gestation, suggesting functional adaptation of the placenta to meet the fetal demands. Here, we show that placental transport of glucose and amino acids are increased in the Igf2 P0 +/- null and that this up-regulation of transport occurs, at least in part, through increased expression of the transporter genes Slc2a3 and Slc38a4 , the imprinted member of the System A amino acid transporter gene family. Decreasing fetal demand genetically by removal of fetal Igf2 abolished up-regulation of both transport systems and reduced placental System A amino acid transport activity and expression of Slc38a2 in late gestation. Our results provide direct evidence that the placenta can respond to fetal demand signals through regulation of expression of specific placental transport systems. Thus, crosstalk between an imprinted growth demand gene ( Igf2 ) and placental supply transporter genes ( Slc38a4 , Slc38a2 , and Slc2a3 ) may be a component of the genetic control of nutrient supply and demand during mammalian development.
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“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 [124]
In the citing paper
“Comparison of the placental-specific Igf2P0 with the complete Igf2 null mutant demonstrates clearly that the small placenta can become more efficient by increasing its nutrient transfer and transporter abundance when there is a maintained drive for growth by feto-placental tissues still expressing Igf2 (124, 125).”
From Placental Origins of Chronic Disease (2016) · cites this paper as [124]
In the citing paper
“Certainly, upregulation of placental amino acid transport is maintained until D19 in mice with complete Igf2P0null litters but not in Igf2P0 mutants of dams with mixed litters of mutants and wild types, which have a greater total conceptus mass and, thus, demand for nutrients in late gestation (124, 495).”
From Placental Origins of Chronic Disease (2016) · cites this paper as [124]
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Self-citation
Metadata
- Authors
- Constância, M., Angiolini, E., Sandovici, I., Smith, P., Smith, R., Kelsey, G., Dean, W., Ferguson-Smith, A., Sibley, C. P., Reik, W., & Fowden, A.
- Affiliations
- Babraham Institute (GB)
- Laboratory of Developmental Genetics and Imprinting, The Babraham Institute, Babraham Research Campus, Cambridge CB2 4AT, United Kingdom; Department of Anatomy, University of Cambridge, Cambridge CB2 3DY, United Kingdom; Division of Human Development, Medical School, University of Manchester, St. Mary's Hospital, Manchester M13 0JH, United Kingdom; and Department of Physiology, University of Cambridge, Cambridge CB2 3EG, United Kingdom
- ORCID
- Venue
- Proceedings of the National Academy of Sciences
- Publisher
- National Academy of Sciences
- Published
- 2005-12-19
- Volume
- 102
- Issue
- 52
- Pages
- 19219-19224
- ISSN
- 0027-8424 (ISSN-L)
- 1091-6490
- PMC
- PMC1316882
- OpenAlex
- W2155091020
- Cited by
- 323
- References
- 34
- Citations by year
- 2026: 4 · 2025: 2 · 2024: 8 · 2023: 6 · 2022: 11 · 2021: 13 · 2020: 17 · 2019: 15 · 2018: 17 · 2017: 12 · 2016: 20 · 2015: 20 · 2014: 16 · 2013: 25 · 2012: 26
- FWCI
- 6.11
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Proceedings of the National Academy of Sciences (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Research Explorer (The University of Manchester) (submittedVersion)
- Funders
- Biotechnology and Biological Sciences Research Council (BBS/E/B/0000S119, BB/B50118X/1, S18929, S18928)
- 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
- insulin-like growth factor II, genomic imprinting, placental nutrient transport, glucose transport, amino acid transport, GLUT3, SLC38A4, SLC38A2, system A, placental development, fetal growth, mice
- MeSH terms
- Alleles, Animals, Biological Transport, Female, Fetus, Genotype, Glucose, Insulin-Like Growth Factor II, Lac Operon, Mice, Inbred C57BL, Models, Genetic, Mutation, Placenta, Proteins, RNA, Messenger, Time Factors, Up-Regulation, Gene Deletion, Genomic Imprinting, Transgenes, Membrane Transport Proteins, Amino Acid Transport Systems, Amino Acid Transport System A, Glucose Transport Proteins, Facilitative, Glucose Transporter Type 3, Mice
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