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First published online on January 24, 2006
Endocrine Reviews, doi:10.1210/er.2005-0011
Endocrine Reviews, doi:10.1210/er.2005-0011
Endocrine Reviews 0 (2006): 200500111-
Copyright © 2006 by The Endocrine Society
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Endocrine regulation of human fetal growth: the role of the mother, placenta and fetus

Vanessa E Murphy, Roger Smith, Warwick B Giles, and Vicki L Clifton*

Mothers and Babies Research Centre, Hunter Medical Research Institute, University of Newcastle, NSW, Australia; Department of Respiratory and Sleep Medicine, Hunter Medical Research Institute, University of Newcastle, NSW, Australia

* To whom correspondence should be addressed. E-mail: vicki.clifton{at}newcastle.edu.au.

The environment in which the fetus develops is critical for its survival and long term health. The regulation of normal human fetal growth involves many multi-directional interactions between the mother, placenta and fetus. The mother supplies nutrients and oxygen to the fetus via the placenta. The fetus influences the provision of maternal nutrients via the placental production of hormones which regulate maternal metabolism. The placenta is the site of exchange between mother and fetus and regulates fetal growth via the production and metabolism of growth regulating hormones such as insulin-like growth factors (IGFs) and glucocorticoids. Adequate trophoblast invasion in early pregnancy and increased uteroplacental blood flow ensure sufficient growth of the uterus, placenta and fetus. The placenta may respond to fetal endocrine signals to increase transport of maternal nutrients by growth of the placenta, by activation of transport systems and by production of placental hormones to influence maternal physiology and even behavior. There are consequences of poor fetal growth both in the short term and long term, in the form of increased mortality and morbidity. Endocrine regulation of fetal growth involves interactions between the mother, placenta and fetus, and these effects may program long term physiology.
Key words: placenta • fetus • insulin-like growth factor • 11{beta}-hydroxysteroid dehydrogenase • low birth weight • fetal programming




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