Cholesterol Transport by the Placenta: Placental Liver X Receptor Activity as a Modulator of Fetal Cholesterol Metabolism?

Influence of altered maternal lipid profile on the lipid profile of the newborn

“…However, the lipoprotein-specific receptors for the transport of fatty acids in the placenta are metabolized in the fetal plasma (6,7,(9)(10)(11)(12). A study conducted with blood from the umbilical cord of newborns showed a lower concentration of TC and lipid fractions when compared with the concentrations obtained in the first days of life of these same individuals, probably due to the production of TC from the maternal milk.…”

“…A study conducted with blood from the umbilical cord of newborns showed a lower concentration of TC and lipid fractions when compared with the concentrations obtained in the first days of life of these same individuals, probably due to the production of TC from the maternal milk. Maternal TC and lipid fractions are transferred to the fetus due to placental permeability (9)(10)(11)(12). However, at the end of the pregnancy, cholesterol is no longer physiologically important, since it is then synthesized by fetal tissues.…”

“…Although the trophoblasts are responsible for the transport of cholesterol to the fetus, these cells express receptors for LDL-c and HDL-c in their membranes, which are responsible for the uptake and transport of cholesterol to the intracellular environment via lysosome. In the lysosome, cholesterol ester is hydrolyzed and then transported by the Niemann-Pick C1 (NPC1) protein, which regulates the transport of cholesterol from the lysosomes to other cellular compartments, making it available to the fetal plasma (9)(10)(11). Despite the occurrence of this transport of lipoproteins from the mother to the fetus, the maternal concentrations of TC, LDL-c, HDL-c and triglycerides seem not to affect the lipid profile of the newborn, as demonstrated in this study.…”

“…The normal physiological increase in circulating lipids allows the mother to have a valuable source of energy for her and for the baby and keeps their metabolic rate steady, enabling the healthy development of the newborn (6). However, during intrauterine development, pathophysiological processes can occur in the metabolism of the lipids leading to abnormal serum concentrations in fetal circulation (7)(8)(9)(10)(11).…”

Role of Nuclear Receptors Peroxisome Proliferator-Activated Receptors (PPARs) and Liver X Receptors (LXRs) in the Human Placental Pathophysiology

“…Depending on the lipidation status of acceptor particles in the fetal circulation, both ABCG1-or ABCA1-dependent pathways seem to be possible, or even a combination of both. Therefore, LXR activation may be considered as a stimulus for increased transport of maternal cholesterol via the placenta to the fetal circulation (Plösch et al,2007). Added to the fact that ABCA1 and ABCG1 are present on the syncytiotropholast (the maternal facing placental membrane), these results identify the inducible placental cholesterol transport by LXR as a preventive mechanism of placental accumulation of cytotoxic oxysterols (Aye et al, 2010).…”