β-Carotene Supplementation Decreases Placental Transcription of LDL Receptor-Related Protein 1 in Wild-Type Mice and Stimulates Placental β-Carotene Uptake in Marginally Vitamin A-Deficient Mice

The human diet contains beta-carotene as the most abundant precursor of vitamin A, an essential nutrient for embryogenesis. Our laboratory previously showed the importance of beta-carotene metabolism via beta-carotene-15,15'-oxygenase (CMOI) to support mouse embryonic development. However, the mechanisms regulating embryonic acquisition and utilization of beta-carotene from the maternal circulation via placenta remain unknown. We used wild-type (WT) and Lrat(-/-) Rbp(-/-) (L-/-R-/-) mice, the latter being a model of marginal vitamin A deficiency. Pregnant dams, fed a nonpurified diet sufficient in vitamin A throughout life, were i.p. supplemented with beta-carotene or vehicle at 13.5 d postcoitum (dpc). Effects of this acute maternal supplementation on retinoid and beta-carotene metabolism in maternal (serum, liver) and developing tissues (placenta, yolk sac, embryo) were investigated at 14.5 dpc. We showed that, upon supplementation, placental beta-carotene concentrations were greater in than in WT mice. However, the retinoid (retinol and retinyl ester) concentrations remained unchanged in placenta (and in all other tissues analyzed) of both genotypes upon beta-carotene administration. We also showed that upon a single i.p. beta-carotene supplementation, placental LDL receptor-related protein (Lrp1) mRNA expression was lower in WT mice, and embryonic Cmol mRNA expression was greater in mice. Together, these data suggest a potential role of LRP1 in mediating the uptake of beta-carotene across the placenta and that even a marginally impaired maternal vitamin A status may influence uptake and utilization of beta-carotene by the placenta and the embryo. J. Nutr. 142: 1456-1462, 2012.