Independent of prepregnancy body mass index (BMI), higher free fatty acid levels during the latter half of pregnancy correlate with birthweight (Crume, 2015). Other studies have correlated mater nal triglyceride levels with birthweight (Di Cianni, 2005; Vrijkotte, 2011). Greater intake of certain fatty acids, particularly omega-3, is also associated with greater birthweight (Calabuig-Navarro, 2016).
Placental fatty acid metabolism and transfer may be dysregulated in fetal-growth restriction and in maternal conditions associated with fetal overgrowth. For example, levels of endothelial lipase are reduced with deicient fetal growth, and this enzyme is overexpressed in placentas of women with diabetes (Gauster, 2007, 2011). Others have reported that diabetes and obesity are associated with altered placental lipid-transport gene expression (Radaelli, 2009). Obesity is also linked with greater expression of fatty acid binding/transport proteins within the trophoblast (Myatt, 2016; Scifres, 2011). he end result of these alterations is an abnormal accumulation of lipids that can result in pathological placental inlammation and dysfunction (Calabuig-Navarro, 2016; Myatt, 2016; Yang, 2016).
mino acids undergo active transport, which explains the normally higher fetal concentrations compared with maternal levels. In growth restriction, this pattern is reversed. One possible mechanism is altered transport of these amino acids. Remember, amino acids that reach the fetus must first cross the microvillus membrane at the maternal interface. Amino acids then traverse the trophoblastic cell, and inally cross the basal membrane into fetal blood (Chap. 5, p. 90). In human placentas, fetal growth correlates with peroxisome proliferator activator receptor gamma (PPAR-,) activity, which governs placental regulation of L-type amino acid (A T) receptors 1 and 2 (Chen, 2015b). Additional modulation is from rap amycin complex (mTORC) 1 and 2 receptors (Rosario, 2013). Placental mTORC activity is reduced in fetal-growth restriction. Others have shown that increasing birthweight and maternal BMI are linked to expression and activity of particular aminoacid transporters at the microvillus membrane (Jansson, 2013).
Normative data for fetal growth based on birthweight vary with ethnicity and geographic region. Accordingly, researchers have developed fetal-growth curves using various populations and geographic locations throughout the United States (Brenner, 1976; Ott, 1993; Overpeck, 1999; Williams, 1975). Because
TABLE 4-1. 2011 Gestational Age Birthweight (g) Percentiles for 3,252,01e1 Singleton Live Births in the United States (Duryea, 2014). hese current curves plot birthweight against a gestational age based on n obsteical estimate, formed in part by sonography. hese curves are thought to be more accurate and reflect more precise pregnancy dating. Older curves used gestational age derived rom a last menstrual period. Comparing birthweights rom 1991 to data from 2011, the more recent growth curves indicate that the earlier assessments overestimated birthweihts in the ase of preterm birth. In particular, the 50th percentile for fetal growth that previ ously corresponded to 31 to 32 weeks' gestation now corresponds to 33 to 34 weeks' when improved obstetrical dating is used.