Placental mTOR links maternal nutrient availability to fetal growth

Author:

Roos Sara1,Powell Theresa L.12,Jansson Thomas12

Affiliation:

1. Perinatal Center, Department of Physiology, Institute of Neuroscience and Physiology, University of Gothenburg, P.O. Box 432, SE-405 30 Gothenburg, Sweden

2. Department of Obstetrics and Gynecology, University of Cincinnati, College of Medicine, 231 Albert B Sabin Way, Cincinnati, OH 45267, U.S.A.

Abstract

The mTOR (mammalian target of rapamycin) signalling pathway functions as a nutrient sensor, both in individual cells and, more globally, in organs such as the fat body in Drosophila and the hypothalamus in the rat. The activity of placental amino acid transporters is decreased in IUGR (intrauterine growth restriction), and recent experimental evidence suggests that these changes contribute directly to the restricted fetal growth. We have shown that mTOR regulates the activity of the placental L-type amino acid transporter system and that placental mTOR activity is decreased in IUGR. The present review summarizes the emerging evidence implicating placental mTOR signalling as a key mechanism linking maternal nutrient and growth factor concentrations to amino acid transport in the human placenta. Since fetal growth is critically dependent on placental nutrient transport, placental mTOR signalling plays an important role in the regulation of fetal growth.

Publisher

Portland Press Ltd.

Subject

Biochemistry

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