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Publication : Embryonic phenotype, β-carotene and retinoid metabolism upon maternal supplementation of β-carotene in a mouse model of severe vitamin A deficiency.

First Author  Wassef L Year  2013
Journal  Arch Biochem Biophys Volume  539
Issue  2 Pages  223-9
PubMed ID  23871845 Mgi Jnum  J:206683
Mgi Id  MGI:5551685 Doi  10.1016/j.abb.2013.07.004
Citation  Wassef L, et al. (2013) Embryonic phenotype, beta-carotene and retinoid metabolism upon maternal supplementation of beta-carotene in a mouse model of severe vitamin A deficiency. Arch Biochem Biophys 539(2):223-9
abstractText  We investigated the effect of beta-carotene (bC) supplementation during pregnancy in a mouse model of severe vitamin A deficiency, i.e. Lrat-/-Rbp-/- dams maintained on a vitamin A-deficient diet during gestation. bC, a provitamin A carotenoid, can be enzymatically cleaved to form vitamin A for use by the developing embryo. We found that an acute supplementation (13.5 days post coitum, dpc) of bC to Lrat-/-Rbp-/- dams on a vitamin A-deficient diet activated transcriptional mechanisms in the developing tissues to maximize the utilization of bC provided to the dams. Nevertheless, these regulatory mechanisms are inefficient under this regimen, as the embryonic phenotype was not improved. We further investigated the effect of a repeated supplementation of bC during a crucial developmental period (6.5-9.5 dpc) on the above-mentioned mouse model. This treatment improved the embryonic abnormalities, as 40% of the embryos showed a normal phenotype. In addition, analysis of retinoic acid-responsive genes, such as Cyp26a1 in these embryos suggests that bC cleavage results in the production of retinoic acid which then can be used by the embryo. Taken together, these in vivo studies show that bC can be used as a source of vitamin A for severely vitamin A-deficient mammalian embryos.
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