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RESEARCH ARTICLE

Environmental regulation of placental phenotype: implications for fetal growth

O. R. Vaughan A B , A. N. Sferruzzi-Perri A , P. M. Coan A and A. L. Fowden A
+ Author Affiliations
- Author Affiliations

A Centre for Trophoblast Research, Department of Physiology, Development and Neuroscience, University of Cambridge, Cambridge CB2 3EG, UK.

B Corresponding author. Email: orv20@cam.ac.uk

Reproduction, Fertility and Development 24(1) 80-96 https://doi.org/10.1071/RD11909
Published: 6 December 2011

Abstract

Environmental conditions during pregnancy determine birthweight, neonatal viability and adult phenotype in human and other animals. In part, these effects may be mediated by the placenta, the principal source of nutrients for fetal development. However, little is known about the environmental regulation of placental phenotype. Generally, placental weight is reduced during suboptimal conditions like maternal malnutrition or hypoxaemia but compensatory adaptations can occur in placental nutrient transport capacity to help maintain fetal growth. In vivo studies show that transplacental glucose and amino acid transfer adapt to the prevailing conditions induced by manipulating maternal calorie intake, dietary composition and hormone exposure. These adaptations are due to changes in placental morphology, metabolism and/or abundance of specific nutrient transporters. This review examines environmental programming of placental phenotype with particular emphasis on placental nutrient transport capacity and its implications for fetal growth, mainly in rodents. It also considers the systemic, cellular and molecular mechanisms involved in signalling environmental cues to the placenta. Ultimately, the ability of the placenta to balance the competing interests of mother and fetus in resource allocation may determine not only the success of pregnancy in producing viable neonates but also the long-term health of the offspring.

Additional keywords: developmental programming, epigenetics, glucocorticoids, insulin-like growth factors, nutrition, system A.


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