High Preformed Vitamin A Intake during Pregnancy Prevents Embryonic Accumulation of Intact β-Carotene from the Maternal Circulation in Mice

The vitamin A precursor β-carotene (BC) promotes mammalian embryonic development by serving as a source of retinoids (vitamin A derivatives) to the developing tissues. In the Western world, increased consumption of dietary supplements, including vitamin A and BC, is common; however, the consequences...

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Published in:The Journal of nutrition 2015-07, Vol.145 (7), p.1408-1414
Main Authors: Wassef, Lesley, Shete, Varsha, Costabile, Brianna, Rodas, Rebeka, Quadro, Loredana
Format: Article
Language:English
Subjects:
Animals
beta Carotene - administration & dosage
beta Carotene - blood
beta Carotene - pharmacokinetics
Dietary Supplements
Embryo, Mammalian - metabolism
Embryonic Development - drug effects
Female
Gene Expression Regulation
Liver - chemistry
Maternal Nutritional Physiological Phenomena
Maternal-Fetal Exchange
Mice
Mice, Inbred C57BL
Placenta - chemistry
Pregnancy
RNA, Messenger - genetics
RNA, Messenger - metabolism
Vitamin A - administration & dosage
Vitamin A - pharmacokinetics
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Summary:The vitamin A precursor β-carotene (BC) promotes mammalian embryonic development by serving as a source of retinoids (vitamin A derivatives) to the developing tissues. In the Western world, increased consumption of dietary supplements, including vitamin A and BC, is common; however, the consequences of maternal high preformed vitamin A intake on embryonic uptake and metabolism of BC are poorly understood. This study investigated vitamin A and BC metabolism in developing mouse tissues after a single BC administration to pregnant wild-type (WT) mice fed purified diets with different vitamin A concentrations. WT dams fed a sufficient vitamin A (VA-S; 4.2 μg of retinol/g of diet), high vitamin A (VA-H; 33 μg of retinol/g of diet), or excess vitamin A (VA-E; 66 μg of retinol/g of diet) diet throughout gestation were intraperitoneally injected with BC or vehicle at 13.5 d postcoitum (dpc). At 14.5 dpc, retinoid and BC concentrations in maternal serum and liver, placenta, and embryo were quantified by HPLC; expressions of genes controlling retinoid and BC homeostasis were analyzed by quantitative polymerase chain reaction. Maternal lipoprotein BC concentrations were analyzed by density gradient ultracentrifugation followed by HPLC. Intact BC was undetectable only in embryos from VA-E + BC dams. Relative to the VA-S + vehicle group, placentas from VA-S + BC dams showed 39% downregulation of LDL-receptor-related protein 1 (Lrp1 ); 35% downregulation of VLDL receptor (Vldlr); 56% reduced mRNA expression of β-carotene 15,15'-oxygenase (Bco1); and 80% upregulation of β-carotene 9',10'-oxygenase (Bco2). Placental cytochrome P450, family 26, subfamily A, polypeptide 1 (Cyp26A1) was upregulated 2-fold in the VA-E group compared with the VA-S group, regardless of maternal treatment. In mice, transfer of intact BC to the embryo is attenuated by high tissue vitamin A concentrations. Maternal vitamin A intake and BC availability activate a placental transcriptional response to protect the embryo from retinoid and carotenoid excess.
ISSN:0022-3166
1541-6100
DOI:10.3945/jn.114.207043