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Maternal‐fetal cholesterol transport in the second half of pregnancy does not involve LRP2 (910.2)
Author(s) -
Zwier Mathijs,
Baardman Maria,
Jurdzinski Angelika,
Bloks Vincent,
Dijk Theo,
Groen Albert,
Plösch Torsten
Publication year - 2014
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.28.1_supplement.910.2
Subject(s) - fetus , probucol , cholesterol , medicine , endocrinology , placenta , in utero , gestation , pregnancy , yolk sac , biology , embryo , genetics , microbiology and biotechnology
Cholesterol is of crucial importance during fetal development and relies on both maternal transport and fetal synthesis. During gestation, Lipoprotein related receptor protein type 2 (Megalin or LRP2) is expressed in both yolk sac and placenta, suggesting a possible role in maternal‐fetal cholesterol transport. Although lipoproteins have been identified as potential LRP2 ligands, the contributing effect of LRP2 on maternal‐fetal cholesterol transport and fetal cholesterol levels in utero have not been adequately addressed. Using stable isotope techniques we quantified maternal‐fetal cholesterol transport in Lrp2 ‐/‐ and WT fetal mice during gestation. Additionally, we administered probucol to half of the dams to reduce maternal cholesterol availability. We found no difference in maternal‐fetal cholesterol transport or synthesis between Lrp2 ‐/‐ and WT littermates, suggesting that LRP2 is not quantitatively involved in maternal‐fetal cholesterol transport. Probucol supplementation lead to a large reduction in maternal plasma cholesterol and was associated with a 50% reduction of maternally derived cholesterol in the fetus, while overall cholesterol levels were unchanged. These results support that the mouse fetus can compensate for decreased maternal cholesterol levels by increasing cholesterol synthesis in utero.