INRA, UMR1260 Nutrition, Obesity and Risk of Thrombosis, Marseille, France.
J Nutr. 2013 Apr;143(4):448-56. doi: 10.3945/jn.112.172734. Epub 2013 Feb 20.
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.
清道夫受体 B 类 I 型(SR-BI)和簇分化抗原 36(CD36)已参与某些维生素原 A 类胡萝卜素的细胞摄取。然而,数据并不完整(例如,没有关于α-胡萝卜素的数据),并且尚不清楚其编码基因中的遗传变异是否会影响维生素原 A 类胡萝卜素的状态。本研究的目的是:1)评估这些清道夫受体在主要维生素原 A 类胡萝卜素(即β-胡萝卜素、α-胡萝卜素和β-隐黄质)以及预形成维生素 A(即视黄醇)的细胞摄取中的作用;2)研究编码这些蛋白的基因中的遗传变异对个体间维生素原 A 类胡萝卜素血浆浓度的差异的影响。在 Caco-2 和人胚肾(HEK)细胞系中研究了 SR-BI 和 CD36 在类胡萝卜素和视黄醇细胞摄取中的作用。通过在 3 个独立人群中的关联研究评估了清道夫受体 B 类 I 型(SCARB1)和 CD36 遗传变异对维生素原 A 类胡萝卜素血浆浓度的影响。细胞实验表明,这两种蛋白都参与了维生素原 A 类胡萝卜素的细胞摄取,但不参与视黄醇的摄取。关联研究表明,在 CD36 和 SCARB1 的单核苷酸多态性和单倍型的不同基因型的参与者之间,几种维生素原 A 类胡萝卜素的血浆浓度存在显著差异(P <0.0083)。结论:SR-BI 和 CD36 参与维生素原 A 类胡萝卜素的细胞摄取,其编码基因中的遗传变异可能在人群水平上调节维生素原 A 类胡萝卜素的血浆浓度。