Regulation of Nutrient Transport across the Placenta

Abstract

Abnormal fetal growth, both growth restriction and overgrowth, is associated with perinatal complications and an increased risk of metabolic and cardiovascular disease later in life. Fetal growth is dependent on nutrient availability, which in turn is related to the capacity of the placenta to transport these nutrients. The activity of a range of nutrient transporters has been reported to be decreased in placentas of growth restricted fetuses, whereas at least some studies indicate that placental nutrient transport is upregulated in fetal overgrowth. These findings suggest that changes in placental nutrient transport may directly contribute to the development of abnormal fetal growth. Detailed information on the mechanisms by which placental nutrient transporters are regulated will therefore help us to better understand how important pregnancy complications develop and may provide a foundation for designing novel intervention strategies. In this paper we will focus on recent studies of regulatory mechanisms that modulate placental transport of amino acids, fatty acids, and glucose.

Oleic acid stimulates system A amino acid transport in primary human trophoblast cells mediated by toll-like receptor 4

“…Placenta from pregnancies complicated by fetal growth restriction have a reduced activity of the amino acid transporters system A and system L ( 18,19 ), whereas these transporter activities are increased in diabetic pregnancies associated with fetal overgrowth ( 7,8 ). The mole cular mechanisms regulating placental amino acid transporters involve multiple signaling pathways ( 20 ). We have previously shown in cultured human primary trophoblast cells that the mammalian target of rapamycin (mTOR) signaling pathway is a positive regulator of system A and system L amino acid transporter activities ( 21 ).…”

Id2 Mediates Differentiation of Labyrinthine Placental Progenitor Cell Line, SM10

“…The placenta is responsible for the transport of nutrients, gases, and wastes between the mother and the fetus [1][2][3][4]. Trophoblast cells that make up the placenta must properly differentiate into the appropriate cell types (lineages) to facilitate this transport [3][4][5][6][7].…”

“…Trophoblast cells that make up the placenta must properly differentiate into the appropriate cell types (lineages) to facilitate this transport [3][4][5][6][7]. Abnormal placental development has been proposed to lead to a reduction in placental function and subsequent pregnancyassociated disorders [1][2][3][4][5][6][7][8].…”

A review of inter- and intraspecific variation in the eutherian placenta

“…The fourth major feature involves the arrangement of the maternal and fetal bloodstreams [4]. This feature partially determines the physiological diffusion efficiency of the various molecules exchanged between mother and fetus [2]. Unfortunately, this feature has not been described in enough mammalian species to reconstruct its evolutionary history accurately.…”

“…The placenta mediates the transfer of nutrients, including oxygen, amino acids, lipids and glucose from the mother to the fetus and provides a method for fetal waste excretion by way of the mother [2]. While these functions are conserved among placental mammals (i.e.…”