| First Author | Wassef L | Year | 2012 |
| Journal | J Nutr | Volume | 142 |
| Issue | 8 | Pages | 1456-62 |
| PubMed ID | 22739378 | Mgi Jnum | J:186392 |
| Mgi Id | MGI:5432267 | Doi | 10.3945/jn.112.162677 |
| Citation | Wassef L, et al. (2012) beta-Carotene Supplementation Decreases Placental Transcription of LDL Receptor-Related Protein 1 in Wild-Type Mice and Stimulates Placental beta-Carotene Uptake in Marginally Vitamin A-Deficient Mice. J Nutr 142(8):1456-62 |
| abstractText | 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 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 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 CmoI mRNA expression was greater in L(-/-)R(-/-) 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. |
