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

Abstract

The human diet contains β-carotene as the most abundant precursor of vitamin A, an essential nutrient for embryogenesis. Our laboratory previously showed the importance of β-carotene metabolism via β-carotene-15, 15'-oxygenase (CMOI) to support mouse embryonic development. However, the mechanisms regulating embryonic acquisition and utilization of β-carotene fromthematernal 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 β-carotene or vehicle at 13.5 d postcoitum (dpc). Effects of this acute maternal supplementation on retinoid and β-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 β-carotene concentrations were greater in L-/-R-/- 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 β-carotene administration. We also showed that upon a single i.p. β-carotene supplementation, placental LDL receptor-related protein (Lrp1) mRNA expression was lower in WT mice, and embryonic CmoImRNA expression was greater in L-/-R-/- mice. Together, these data suggest a potential role of LRP1 inmediating the uptake of β-carotene across the placenta and that even amarginally impairedmaternal vitamin A status may influence uptake and utilization of β-carotene by the placenta and the embryo. © 2012 American Society for Nutrition.