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Placental phenotype and the insulin-like growth factors: resource allocation to fetal growth

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Peer-reviewed

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Type

Article

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Authors

Sferruzzi-Perri, AN 
Fowden, AL 

Abstract

The placenta is the main determinant of fetal growth and development in utero. It supplies all the nutrients and oxygen required for fetal growth and secretes hormones that facilitate maternal allocation of nutrients to the fetus. Furthermore, the placenta responds to nutritional and metabolic signals in the mother by altering its structural and functional phenotype which can lead to changes in maternal resource allocation to the fetus. The molecular mechanisms by which the placenta senses and responds to environmental cues are poorly understood. This review discusses the role of the insulin-like growth factors (IGFs) in controlling placental resource allocation to fetal growth, particularly in response to adverse gestational environments. In particular, it assesses the impact of the IGFs and their signalling machinery on placental morphogenesis, substrate transport and hormone secretion, primarily in the laboratory species, although it draws on data from human and other species where relevant. It also considers the role of the IGFs as environmental signals in linking resource availability, to fetal growth through changes in the morphological and functional phenotype of the placenta. As altered fetal growth is associated with increased perinatal morbidity and mortality and a greater risk of developing adult-onset diseases in later life, understanding the role of IGFs during pregnancy in regulating placental resource allocation to fetal growth is important for identifying the mechanisms underlying the developmental programming of offspring phenotype by suboptimal intrauterine growth.

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Keywords

resource allocation, fetus, placenta, IGF, pregnancy, nutrient transport, signalling

Journal Title

Journal of Physiology

Conference Name

Journal ISSN

0022-3751
1469-7793

Volume Title

Publisher

Wiley
Sponsorship
Biotechnology and Biological Sciences Research Council (BB/I014594/1)
ANS-P is funded by a Royal Society Dorothy Hodgkin Research Fellowship.
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