The placental uptake and use ofLDL is an alternative mechanism for fetal assimilation of essential fatty acids and amino acids (Chap. 5, p. 103). LDL binds to specific receptors in the coated-pit regions of the syncytiotrophoblast microvilli. The large LDL particle, measuring about 250,000 Da, is taken up by a process of receptor-mediated endocytosis. The apoprotein and cholesterol esters of LD L are hydrolyzed by lysosomal enzymes in the syncytium to yield: (1) cholesterol for progesterone synthesis; (2) free amino acids, including essential amino acids; and (3) essential fatty acids, primarily linoleic acid.
he placenta concentrates many amino acids in the syncytiotrophoblast, which are then transferred to the fetal side by difusion. Based on data from cordocentesis blood samples, the amino acid concentration in umbilical cord plasma is greater than in maternal venous or arterial plasma (Morriss, 1994) . Transport system activity is influenced by gestational age and environmental factors. hese include heat stress, hypoxia, under-and overnutrition, and hormones such as glucocorticoids, growth hormone, and leptin (Brifa, 2015; Fowden, 2006). Trophoblastic mammalian target of rapamycin complex 1 (mTORC1) regulates placental amino acid transporters and modulates transfer across the placenta Qansson, 2012). In vivo studies suggest an upregulation of transport for certain amino acids and a greater delivery rate of these to the fetuses of women with gestational diabetes associated with fetal overgrowth Oansson, 2006a).
Placental transfer of larger proteins is limited, but there are exceptions. IgG crosses the placenta in large amounts via endocytosis and trophoblast Fc receptors. IgG transfer depends on maternal levels of total IgG, gestational age, placental integrity, IgG subclass, and antigenic potential (Palmeira, 2012). Conversely, the larger immunoglobulins-IgA and IgM-of maternal origin are efectively excluded from the fetus.
Calcium and phosphorus are actively transported from mother to fetus. Calcium is transferred for fetal skeletal mineralization (Olausson, 2012). A calcium-binding protein is produced in placenta. Parathyroid hormone-related protein (PTH-rP), as the name implies, acts as a surrogate PTH in many systems (Chap. 5, p. 102). PTH is not found in fetal plasma, but PTHrP is present, suggesting that PTH-rP is the fetal parathormone. The expression of PTH-rP in cytotrophoblasts is modulated by the extracellular concentration of Ca2+ (Hellman, 1992). It seems possible, therefore, that PTH-rP synthesized in decidua, placenta, and other fetal tissues is important in fetal Cai+ transfer and homeostasis.
Iodide transport is clearly attributable to a carrier-mediated, energy-requiring active process. And indeed, the placenta concentrates iodide. he concentrations of zinc in the fetal plasma also are greater than those in maternal plasma. Conversely, copper levels in fetal plasma are less than those in maternal plasma. his fact is of particular interest because important copperrequiring enzymes are necessary for fetal development.