Gestational Age Dependency of Essential Fatty Acids in Cord Plasma Cholesterol Esters and Triglycerides

Abstract

ABSTRACT. Plasma cholesterol ester and triglyceride fatty acid compositions of 38 singleton deliveries (23-42 wk), three twins (32, 39, and 40 wk), and their mothers were investigated. No gestational age-dependent changes occurred in maternal fatty acid compositions. Long-chain polyunsaturated fatty acids in fetal cholesterol esters and triglycerides were higher, and their precursors (18:2c,w6 and 18:3c,w3) were lower than those in corresponding maternal lipid classes. Except for 22:6c,w3, 20:2c,w6, and 22:5c,w6, all long-chain polyunsaturated fatty acids in fetal triglycerides increased with advancing gestation. Fetal triglyceride 22:6c,w3/22:5c,w3 ratio decreased, whereas 22:5c,w6/22:4c,w6 remained constant. Fetal cholesterol ester and triglyceride 20:3c,w9 contents were higher than those of corresponding maternal fractions and did not change with gestation. Triglyceride 18:2c,w6 contents of babies with gestational ages of more than 34 wk were linearly related to those of their mothers. The data suggest that increasing triglyceride long-chain polyunsaturated fatty acid content with advancing gestation is partially caused by a6-and a5-desaturase maturation in the liver. 22:6c,w3 and 22:5c,w6/22:4c,w6 and decrease of 22:6c,w3/22:5c,w3 in triglycerides may point to low hepatic a4-desaturation. Transplacental transport of 20:3c,w9, followed by fetal conservation, should be considered. High 18:2c,w6 and low 18:3c,w3 intakes by the mother may unfavorably influence fetal production of 22:6c,w3 in the liver. Because of low hepatic a4-desaturation capacity the influence may be small, however. iPediatr Res 35: 461-469, 1994) Abbreviations CE, cholesterol ester TG, triglyceride FA, fatty acid LCPUFA, long-chain polyunsaturated fatty acid EF A, essential fatty acid LCAT, lecithin:cholesterol acyltransferase PC, phosphatidylcholine AFP, a-fetoprotein Constancy ofThe parent EFA, linoleic (18:2c,w6) and a-linolenic (18:3c,w3) acids, are partially converted into LCPUFA with 20 carbon atoms or more. LCPUFA biosynthetic routes comprise altema-

Intrauterine Growth Restriction Is Associated with Changes in Polyunsaturated Fatty Acid Fetal-Maternal Relationships

“…This is in agreement with a number of previous studies reporting that the proportions of AA and DHA are sharply increased across the placenta in term pregnancies (17,18,(23)(24)(25)(26). Both total and relative maternal fatty acid concentrations did not change in the range of gestation studied, confirming that most changes in maternal plasma fatty acid composition occur in the first half of pregnancy (27).…”

Age- and Dietary-Related Distributions of Hepatic Arachidonic and Docosahexaenoic Acid in Early Infancy

“…It may be that only after approximately 12 wk is optimal hepatic synthesis of DHA evinced and that irrespective of dietary provision of a-linolenic acid, A4-desaturation is poorly or nonfunctioning in early life. This appears to corroborate recent observations on cord plasma fatty acids which seein to demonstrate that A4-desaturation and not A6 or A5 may be rate-limiting in the formation of hepatic DHA (22). If as indicated A4-desaturation is achieved through microsomal chain elongation of docosapentaenoic acid [C22:5(n-3)] followed by A6-desaturation then the final peroxisomal @-oxidation may be the true rate-limiting step to DHA production in the infant liver (21).…”

Effect of placental function on fatty acid requirements during pregnancy

“…Longitudinal data on maternal and umbilical blood phospholipid fatty acid composition from Al et al (1995Al et al ( , 2000 indicate that, as with total fat deposition in the fetus, DHA as a percent of total fatty acids in the fetal blood increases exponentially after around 20 weeks gestation. This appears to be a general phenomenon with the DHA percent also increasing in the cholesterol ester (CE) fraction and AA, LA and aLN increasing in the CE and TG fractions at this time (Hoving et al, 1994). This trans-placental gradient is critical to the delivery of n-3/ n-6 fatty acids to the fetus and there are multiple mechanisms within the placenta to bring it about.…”

“…Figure 2 Fatty acids may be found in the blood and tissues linked to other molecules by ester bonds; triglyceride (TG), phospholipid (PL) and cholesterol ester (CE); or as non-esterified fatty acids NEFA. AA and DHA as a proportion of total fatty acids are shown for the diet of pregnant mothers (Lakin et al, 1998), 1 the adipose tissue (Leaf et al, 1995), 2 maternal and cord blood plasma phospholipids (Otto et al, 1997), 3 triglyceride (Berghaus et al, 2000), 4 cholesterol ester (Hoving et al, 1994), 5 and NEFA (Benassayag et al, 1999), 6 the placental microvillous and basal membranes (Powell et al, 1999), 7 and adipose tissue and brain at birth (Clandinin et al, 1981 Figure 3 The theoretical rate of oxidation was calculated from the rate of maternal energy expenditure (9453 MJ/day), the proportion of that energy derived from fat (30%), the energy content of fat (39 kJ/g) (Butte, 2000) and the proportion of DHA in the oxidised fat (0.1% DHA; Figure 2). The DHA content of fetal tissues was calculated from the lean mass (calculated as body weight minus the weight of fat, skeleton and skin (Widdowson, 1974)), the fat mass (Widdowson, 1974) and the weight of the placenta (Hytten, 1974) and brain (Clandinin et al, 1980) and the fat and DHA concentration of the brain (Clandinin et al, 1980;Jamieson et al, 1999), placenta (Widdowson & Spray, 1951;Lakin et al, 1998) and adipose tissue (Clandinin et al, 1981).…”