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Role of LDL receptor in the uptake of beta‐carotene by murine placenta and the embryo
Author(s) -
Shete Varsha,
Costabile Brianna,
Quadro Loredana
Publication year - 2013
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.27.1_supplement.32.5
Subject(s) - ldl receptor , placenta , endocrinology , medicine , embryo , biology , apolipoprotein b , knockout mouse , fetus , very low density lipoprotein , receptor , embryogenesis , apolipoprotein e , andrology , lipoprotein , cholesterol , pregnancy , genetics , disease
Beta‐carotene (bC) is the most abundant precursor of vitamin A in the human diet. Vitamin A derived retinoids are essential for normal embryonic development. Uptake of intact bC followed by local de novo biosynthesis of retinoids by cleavage of bC can be an important source of retinoids during embryonic development. Intact bC is circulated in association with various lipoprotein particles, especially apoE/apoB containing lipoproteins such as chylomicrons, VLDL and LDL. Potential role of LDL receptor (LDLr) in the uptake of supplemented bC by maternal and developing tissues was investigated. LDLr knockout female mice were mated with LDLr heterozygous males and vice versa to obtain embryos of the same litter that are either heterozygous or lack LDLr altogether. All mice were maintained on a regular chow diet throughout the lifespan. At 13.5 days of gestation, dams were intraperitoneally supplemented with a physiological dose of 20–50 μg/g body weight of bC. Maternal serum, liver, placenta and embryos were collected after 24 hours and analyzed by HPLC and qPCR. Hepatic bC levels were reduced in LDLr knockout dams. Placenta of heterozygous embryos had higher bC levels as compared to the knockout placenta, an effect observed only in case of LDLr knockout dams. Maternal and embryonic genotype did not have an effect on bC levels in embryos. Preliminary qPCR analysis of placenta revealed that both bC supplementation and LDLr genotype of the placenta had an effect on the mRNA expression of genes involved in lipid metabolism. These results suggest that LDLr mediates uptake of bC 1) in the liver and 2) in the placenta of dams lacking LDLr. In addition to this, the data suggested that a single dose of bC at mid‐gestation may alter genes involved in the lipid metabolism in the placenta and the embryo. Grant Funding Source : NIH

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