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Nutrients. 2015 Jan 8;7(1):360-89. doi: 10.3390/nu7010360.

Placental adaptations in growth restriction.

Author information

1
Early Origins of Adult Health Research Group, Sansom Institute for Health Research, University of South Australia, Adelaide, SA 5001, Australia. song.zhang@unisa.edu.au.
2
Departments of Obstetrics and Gynecology, University of Western Ontario, London, ON N6A 5C1, Canada. tim.regnault@uwo.ca.
3
Early Origins of Adult Health Research Group, Sansom Institute for Health Research, University of South Australia, Adelaide, SA 5001, Australia. barpl002@mymail.unisa.edu.au.
4
Early Origins of Adult Health Research Group, Sansom Institute for Health Research, University of South Australia, Adelaide, SA 5001, Australia. kb555@cam.ac.uk.
5
Early Origins of Adult Health Research Group, Sansom Institute for Health Research, University of South Australia, Adelaide, SA 5001, Australia. caroline.mcMillen@newcastle.edu.au.
6
Early Origins of Adult Health Research Group, Sansom Institute for Health Research, University of South Australia, Adelaide, SA 5001, Australia. mcmcm003@mymail.unisa.edu.au.
7
The Robinson Research Institute, University of Adelaide, Adelaide, SA 5005, Australia. claire.roberts@adelaide.edu.au.
8
Early Origins of Adult Health Research Group, Sansom Institute for Health Research, University of South Australia, Adelaide, SA 5001, Australia. janna.morrison@unisa.edu.au.

Abstract

The placenta is the primary interface between the fetus and mother and plays an important role in maintaining fetal development and growth by facilitating the transfer of substrates and participating in modulating the maternal immune response to prevent immunological rejection of the conceptus. The major substrates required for fetal growth include oxygen, glucose, amino acids and fatty acids, and their transport processes depend on morphological characteristics of the placenta, such as placental size, morphology, blood flow and vascularity. Other factors including insulin-like growth factors, apoptosis, autophagy and glucocorticoid exposure also affect placental growth and substrate transport capacity. Intrauterine growth restriction (IUGR) is often a consequence of insufficiency, and is associated with a high incidence of perinatal morbidity and mortality, as well as increased risk of cardiovascular and metabolic diseases in later life. Several different experimental methods have been used to induce placental insufficiency and IUGR in animal models and a range of factors that regulate placental growth and substrate transport capacity have been demonstrated. While no model system completely recapitulates human IUGR, these animal models allow us to carefully dissect cellular and molecular mechanisms to improve our understanding and facilitate development of therapeutic interventions.

PMID:
25580812
PMCID:
PMC4303845
DOI:
10.3390/nu7010360
[Indexed for MEDLINE]
Free PMC Article

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