Abstract
Background/objectiveAn adequate supply of long-chain polyunsaturated fatty acids (LC PUFA) promotes foetal health and development, whereas generally, trans fatty acids (tFA) are considered to negatively interfere with LC PUFA metabolism. Nevertheless, to date, limited data concerning separate trans C18:1, such as t9 and t11, are available for maternal and foetal blood. Therefore, in this study the portions of individual trans C18:1, LC n-6, and n-3 PUFA in lipids of maternal and foetal plasma and erythrocyte membranes of German mother and child pairs (n=40) were analysed.ResultsPortions of linoleic acid and α-linolenic acid as LC precursors were lower (~0.4-fold); whereas the metabolites arachidonic acid (AA, n-6) and docosahexaenoic acid (DHA, n-3) were significantly higher (~2-fold) in foetal than in maternal plasma and erythrocytes. The main tFA in maternal and foetal blood were elaidic acid (C18:1t9; t9) and vaccenic acid (C18:1t11; t11). Portions of t9, t10, t11, and t12 in foetal blood lipids were lower (~0.5-fold) compared with maternal blood. In foetal lipids, t9 was higher than t11. The t9 correlated negatively with eicosapentaenoic acid (n-3) and AA in maternal and foetal lipids; whereas t11 correlated negatively only with foetal total LC n-6 (plasma and erythrocytes) and n-3 PUFA (erythrocytes). No correlation between maternal tFA and foetal PUFA was observed.Conclusions‘Biomagnification’ of LC n-6 and n-3 PUFA AA and DHA in foetal blood was confirmed, whereas single trans isomers were lower compared with maternal blood. Nevertheless, tFA intake, especially from industrial sources, should be as low as possible.
Highlights
The essential dietary fatty acids (FA) linoleic acid (C18:2 n-6; LA) and a-linolenic acid (C18:3 n-3; ALA) are necessary for the endogenous synthesis of the long-chain polyunsaturated fatty acids (LC PUFA) arachidonic acid (C20:4 n-6; AA) and docosahexaenoic acid (C22:6 n-3; DHA) [1]
Trans fatty acids in foetal tissue are exclusively derived from the maternal diet, perinatal by placental transport and postnatal by breast milk [7, 15]. tFA are considered to exhibit adverse effects on essential FA and LC PUFA metabolism
The intake of essential FA can be reduced by the competition of tFA and essential FA or PUFA, respectively, which can result in negative effects regarding foetal and infant development [16]
Summary
The essential dietary fatty acids (FA) linoleic acid (C18:2 n-6; LA) and a-linolenic acid (C18:3 n-3; ALA) are necessary for the endogenous synthesis of the long-chain polyunsaturated fatty acids (LC PUFA) arachidonic acid (C20:4 n-6; AA) and docosahexaenoic acid (C22:6 n-3; DHA) [1] These metabolites, DHA, are important structural components, such as of cell membranes of the retina and the nervous system, suggesting an essential role for foetal and infant brain development [1]. Trans fatty acids (tFA) in foetal tissue are exclusively derived from the maternal diet, perinatal by placental transport and postnatal by breast milk [7, 15]. The FA profiles including single trans C18:1 isomers were determined in maternal and foetal plasma and the respective erythrocyte membranes as well as in milk samples
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