Maternal Lipid Metabolism and Placental Lipid Transfer

Abstract

During early pregnancy, long-chain polyunsaturated fatty acids (LC-PUFA) may accumulate in maternal fat depots and become available for placental transfer during late pregnancy, when the fetal growth rate is maximal and fetal requirements for LC-PUFAs are greatly enhanced. During this late part of gestation, enhanced lipolytic activity in adipose tissue contributes to the development of maternal hyperlipidaemia; there is an increase in plasma triacylglycerol concentrations, with smaller rises in phospholipid and cholesterol concentrations. Besides the increase in plasma very-low-density lipoprotein, there is a proportional enrichment of triacylglycerols in both low-density lipoproteins and high-density lipoproteins. These lipoproteins transport LC-PUFA in the maternal circulation. The presence of lipoprotein receptors in the placenta allows their placental uptake, where they are hydrolysed by lipoprotein lipase, phospholipase A₂ and intracellular lipase. The fatty acids that are released can be metabolized and diffuse into the fetal plasma. Although present in smaller proportions, maternal plasma non-esterified fatty acids are also a source of LC-PUFA for the fetus, their placental transfer being facilitated by the presence of a membrane fatty acid-binding protein. There is very little placental transfer of glycerol, whereas the transfer of ketone bodies may become quantitatively important under conditions of maternal hyperketonaemia, such as during fasting, a high-fat diet or diabetes. The demands for cholesterol in the fetus are high, but whereas maternal cholesterol substantially contributes to fetal cholesterol during early pregnancy, fetal cholesterol biosynthesis rather than cholesterol transfer from maternal lipoproteins seems to be the main mechanism for satisfying fetal requirements during late pregnancy.

Effect of Gestational Diabetes on Circulating Levels of Maternal and Neonatal Carnitine

“…Moreover, our findings support the view that the excess of lipids is not used by the mother but it is rather transferred to the fetus. The transport of FAs to the fetus is facilitated by the presence of lipoprotein receptors together with lipoprotein lipase, phospholipase A2, and intracellular lipases in the placenta, which allow the free FAs to be released from maternal lipoproteins and triglycerides, transferred through the placenta and utilized by the fetus [18,19]. This process is very important for normal fetal development, which requires the availability of essential FAs and long-chain polyunsaturated FAs for growth and development [20].…”

Fatty Acids as Biocompounds: Their Role in Human Metabolism, Health and Disease - A Review. Part 2: Fatty Acid Physiological Roles and Applications in Human Health and Disease

“…These can be re-esterified and stored, and then hydrolysed and released into the fetal bloodstream 68 . Transport of LC PUFA to the placenta is mainly done by uptake of maternal TAG intact in plasma 73 . This is suggested to be greater than uptake of NEFA from the placenta.…”

Association of hyperlipidemia in preterm delivery

“…Plasma cholesterol and triglycerides may increase by 25% to 50% and 150% to 300% respectively. [6][7][8] Atherosis of the utero placental spiral arteries may be induced by the Hyperlipidemia in pregnancy. Atherosis of the vital placental arteries combined with hyper coagulation may result in thrombosis and placental infarctions, leading to placental insufficiency and thereby fetal compromise.…”