The major function of the placenta is the promotion of fetal growth and viability. One of the ways by which it achieves this goal is by ensuring adequate nutrient supply from the mother to the fetus, with the placenta representing the interface between the two. The exchange of nutrients, gases, and metabolic waste products between the maternal and fetal circulations occurs across this interface. In humans, the trophoblasts, which constitute the functional unit of the placenta, are not in direct contact with maternal blood during the early stages of placentation (until 10-12 weeks of gestation), and the nutrients for the fetal growth are obtained mainly from the secretions of the uterine glands in the endometrium (1-3). Thus, the fetus during early stages of development is said to have histiotrophic nutrition. With the completion of implantation and the development of the definitive placenta, direct contact between the trophoblasts and thematernal blood is established. From this stage onward, the fetus derives its nutrition directly from the maternal circulation and is thus said to have hemotrophic nutrition. Fetal growth and development are intimately linked to the transport functions of the placenta, which is a metabolically active tissue rather than a simple permeable barrier. While some nutrients are transported unaltered through the trophoblasts, themajority of the nutrients are either partially consumed or metabolized to other molecules by the placenta. In addition to the transcellular pathway of nutrient flux, the presence of extracellular/paracellular pathways for transplacental nutrient ux has also been reported (4-6). However, due to the lack of morphological evidence, the quantitative and qualitative importance of such pathways to overall nutrient flux is still a MD: BHATIA, JOB: 04362, matter of debate. Transplacental transport can be classiffied into four groups: (1) simple di?usion: transport down a concentration gradient without participation of any transport protein and expenditure of metabolic energy; (2) facilitated diffuusion: transport down a concentration gradient without the expense of metabolic energy but with participation of specific transport protein; (3) active transport: transport against a concentration gradient, mediated by specific transport proteins and driven by one or more forms of metabolic energy; and (4) receptor-mediated endocytosis: transport involving specific cell surface receptors and clathrin-coated pit-or caveolae-mediated endocytosis. Recent progress inmolecular biology has yielded awealth of new information on the mechanisms of transplacental nutrient transport and its regulation. The purpose of this chapter is to summarize the current understanding of the cellular, molecular, and regulatory mechanisms underlying the placental transport of important nutrients that are essential for optimal growth and development of the fetus.
|Original language||English (US)|
|Title of host publication||Perinatal Nutrition|
|Subtitle of host publication||Optimizing Infant Health and Development|
|Number of pages||34|
|State||Published - Jan 1 2004|
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