Differential Long-Chain Polyunsaturated Fatty Acids Status and Placental Transport in Adolescent Pregnancies

Abstract

Adolescent pregnancy increases risk of adverse perinatal outcomes. Placental delivery of long-chain polyunsaturated fatty acids (LCPUFA) is essential for fetal growth and development. In this pilot study, we aimed to assess maternal and fetal status of fatty acids (FA) measured at birth and the expression of key genes involved in FA uptake, transport and metabolism in the placenta of fifteen adolescents and fifteen adults. FA were quantified by gas-liquid chromatography. Placental expression of FA transporters was assessed by quantitative real-time polymerase chain reaction (qRT-PCR) and peroxisome proliferator-activated receptor gamma (PPARγ) was quantified by Western Blot. Adolescents had lower docosahexaenoic acid (DHA, 22:6 n-3) and total n-3 FA levels in maternal erythrocytes and placenta, but these were not different in fetal erythrocytes. Arachidonic acid (AA, 20:4 n-6) concentration was increased in placenta but lower in fetal circulation. Plasma membrane fatty acid binding protein (FABPpm) and fatty acid transport protein (FATP) 4 mRNA expressions were not different, however FATP1, fatty acid translocase (FAT/CD36) and fatty acid binding protein 3 (FABP3) mRNA and PPARγ protein levels were decreased in placenta of adolescents. Despite significant downregulation of FATP1, CD36 and FABP3, there was only a modest decrease in LCPUFA (10%) and AA (12%) and no difference in DHA content in cord blood, suggesting that FA transfer to the fetus was partially protected by other factors in adolescents from this cohort.

Maternal dietary fatty acids and their roles in human placental development

“…It further led to a decrease in placental inflammation and upregulated the expression of fatty acid transporting protein 4 proteins in the placenta [79]. In adolescent pregnancies, placental FATP1, CD36 and FABP3 expression were significantly downregulated with a modest decrease in overall LCPUFA (10%) levels without affecting cord blood DHA levels [80].…”

Association of MTHFR (C677T, A1298C) and MTRR A66G polymorphisms with fatty acids profile and risk of neural tube defects

“…An adequate amount of PUFA, particularly n‐3 PUFA and n‐6 PUFA, must be transferred from the mother to the child via the placenta for appropriate growth and development (Fonseca et al, 2018).…”

“…PUFA play an important role in the placenta's regulation of oxidative stress, angiogenesis, and inflammation (Rani et al, 2015). For proper growth and development, a sufficient amount of PUFA, particularly n‐3 PUFA and n‐6 PUFA, must be transferred from the mother to the child via the placenta (Fonseca et al, 2018).…”

Intrauterine Transfer of Polyunsaturated Fatty Acids in Mother–Infant Dyads as Analyzed at Time of Delivery

“…However, micronutrients that may be subject to tighter regulation have shown correlation to fetal growth such as retinol, which is essential during pregnancy to support fetal growth [ 7 ]. Placental PUFA transfer appears to rely largely on plasma membrane bound proteins that bind non-esterified fatty acids and transport them across the membrane, with a small number of fatty acids being able to cross the placental membrane via passive diffusion [ 8 ]. Since the maternal to fetal gradient of free fatty acids is high, some passive diffusion can occur; however, these fatty acids are processed and esterified prior to release into the fetal circulation [ 9 ].…”