Maternal High Linoleic Acid Alters Placental Fatty Acid Composition

Abstract

Fetal development is modulated by maternal nutrition during pregnancy. The dietary intake of linoleic acid (LA), an essential dietary n-6 polyunsaturated fatty acid (PUFA), has increased. We previously published that increased LA consumption during pregnancy does not alter offspring or placental weight but fetal plasma fatty acid composition; the developing fetus obtains their required PUFA from the maternal circulation. However, it is unknown if increased maternal linoleic acid alters placental fatty acid storage, metabolism, transport, and general placental function. Female Wistar-Kyoto rats were fed either a low LA diet (LLA; 1.44% of energy from LA) or high LA diet (HLA; 6.21% of energy from LA) for 10 weeks before pregnancy and during gestation. Rats were sacrificed at embryonic day 20 (E20, term = 22 days) and placentae collected. The labyrinth of placentae from one male and one female fetus from each litter were analyzed. High maternal LA consumption increased placental total n-6 and LA concentrations, and decreased total n-3 PUFA, alpha-linolenic acid (ALA), and docosahexaenoic acid (DHA). Fatty acid desaturase 1 (Fads1), angiopoietin-like 4 (Angptl4), and diacylglycerol lipase beta (Daglb) mRNA were downregulated in placentae from offspring from HLA dams. Maternal high LA downregulated the fatty acid transport protein 4 (Fatp4) and glucose transporter 1 (Slc2a1) mRNA in placentae. IL-7 and IL-10 protein were decreased in placentae from offspring from HLA dams. In conclusion, a high maternal LA diet alters the placental fatty acid composition, inflammatory proteins, and expressions of nutrient transporters, which may program deleterious outcomes in offspring.

Maternal Vitamin and Mineral Supplementation and Rate of Maternal Weight Gain Affects Placental Expression of Energy Metabolism and Transport-Related Genes

“…Underlying the fatty acid metabolism pathway, we identified FADS1 and ACAT2 as DEG for CAR. The FADS1 gene codes for a rate-limiting enzyme involved with the metabolism and degradation of polyunsaturated fatty acids, such as docosahexaenoic acid and arachidonic acid [ 43 ]. Likewise, the protein encoded by ACAT2 acts in lipid biosynthesis and regulates the synthesis of cholesteryl ester [ 44 ].…”

Impact of Maternal Obesity on the Metabolism and Bioavailability of Polyunsaturated Fatty Acids during Pregnancy and Breastfeeding

“…Interestingly, in vitro models have shown that high levels of DHA (100 µM) enhance lipid peroxidation and DNA oxidative damage in placental cells and explants [ 105 ]. On the other hand, pregnant rats fed with a LA-rich diet showed decreased placental concentrations of IL-7 and IL-10, indicating that this n -6 PUFA has both pro-inflammatory and anti-inflammatory properties in the placenta [ 106 ]. DHA seems to have beneficial effects on fetal growth but no effects on placental tissue in rat models.…”

Maternal Factors Associated with Levels of Fatty Acids, Specifically n-3 PUFA during Pregnancy: ECLIPSES Study

“…An optimal long-chain n-3 fatty acid status during pregnancy is of particular benefit for cognitive and visual development of the foetus [4][5][6], and is linked to a reduction in the numbers of preterm births and low birth weights, and a reduced risk of preeclampsia and postpartum depression for the mother [1,7,8]. Furthermore, although linoleic acid (LA), omega-6 polyunsaturated fatty acid (n-6 PUFA), is an essential fatty acid, it is suggested that an adequate balance with n-3 is necessary since high levels of n-6 before or during pregnancy may have negative effects on foetal development and may influence the overall health of offspring in later stages of life [9,10].…”