Uptake of beta‐carotene by the maternal‐fetal barrier: influences of maternal vitamin A regimens and its mechanisms

Synthesis of vitamin A by cleavage of β‐carotene, its most abundant precursor in human diet, is regulated by nutrient availability in adult tissues. Intact β‐carotene is transported in association with various lipoprotein particles in circulation. Local de novo biosynthesis of retinoids from β‐carotene can be an important source of retinoids during embryonic development. Retinoids, especially transcriptionally active retinoic acid, are essential for normal embryonic development. This study examines effects of different maternal vitamin A regimens on uptake of supplemented β‐carotene by maternal‐fetal barrier. Wild‐type mice were maintained on diets containing sufficient, deficient and excess amounts of vitamin A during pregnancy. At 13.5 days of gestation, dams were supplemented with 10–30 μg/gbody weight of β‐carotene by intraperitonial injection. Maternal serum, liver, placenta, embryos were collected after 24 hours and analyzed by HPLC. Pregnant females injected with vehicle were controls. Well detectable β‐carotene levels were observed in maternal serum, liver, placenta and embryos in all supplemented mice. Serum and liver β‐carotene levels were unaltered under different vitamin A regimens. Embryonic β‐carotene levels were reduced when dams were maintained on vitamin A‐excess diet, but placental levels were not altered under any of the dietary regimens. This suggests a protective action of placenta that limits the transfer of β‐carotene from maternal circulation to embryo under vitamin A excess conditions. mRNA expressions of placental LDL receptor, SRBI (HDL receptor) were unchanged upon β‐carotene supplementation, however LRP1 (chylomicron remnants receptor) was dramatically downregulated upon β‐carotene supplementation, at least when dams were on vitamin A‐sufficient diet. Grant Funding Source : NIH