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CD36 and SR-BI Are Involved in Cellular Uptake of Provitamin A Carotenoids by Caco-2 and HEK Cells, and Some of Their Genetic Variants Are Associated with Plasma Concentrations of These Micronutrients in Humans

2013; Elsevier BV; Volume: 143; Issue: 4 Linguagem: Inglês

10.3945/jn.112.172734

1541-6100

Patrick Borel, Georg Lietz, Aurélie Goncalves, Fabien Szabo de Edelenyi, Sophie Lecompte, Peter J. Curtis, Louisa Goumidi, Muriel Caslake, Elizabeth A. Miles, Christopher J. Packard, Philip C. Calder, John C. Mathers, Anne Marie Minihane, Franck Tourniaire, Emmanuelle Kesse‐Guyot, Pilar Galán, Serge Herçberg, Christina Breidenassel, Marcela González‐Gross, Myriam Moussa, Aline Meirhaeghe, Emmanuelle Reboul,

Retinoids in leukemia and cellular processes

Scavenger receptor class B type I (SR-BI) and cluster determinant 36 (CD36) have been involved in cellular uptake of some provitamin A carotenoids. However, data are incomplete (e.g., there are no data on α-carotene), and it is not known whether genetic variants in their encoding genes can affect provitamin A carotenoid status. The objectives were 1) to assess the involvement of these scavenger receptors in cellular uptake of the main provitamin A carotenoids (i.e., β-carotene, α-carotene, and β-cryptoxanthin) as well as that of preformed vitamin A (i.e., retinol) and 2) to investigate the contribution of genetic variations in genes encoding these proteins to interindividual variations in plasma concentrations of provitamin A carotenoids. The involvement of SR-BI and CD36 in carotenoids and retinol cellular uptake was investigated in Caco-2 and human embryonic kidney (HEK) cell lines. The involvement of scavenger receptor class B type I (SCARB1) and CD36 genetic variants on plasma concentrations of provitamin A carotenoids was assessed by association studies in 3 independent populations. Cell experiments suggested the involvement of both proteins in cellular uptake of provitamin A carotenoids but not in that of retinol. Association studies showed that several plasma provitamin A carotenoid concentrations were significantly different (P < 0.0083) between participants who bore different genotypes at single nucleotide polymorphisms and haplotypes in CD36 and SCARB1. In conclusion, SR-BI and CD36 are involved in cellular uptake of provitamin A carotenoids, and genetic variations in their encoding genes may modulate plasma concentrations of provitamin A carotenoids at a population level.