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CD36 和 SR-BI 参与了 Caco-2 和 HEK 细胞对类维生素 A 胡萝卜素的细胞摄取,它们的一些遗传变异与人体中这些微量营养素的血浆浓度有关。

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.

机构信息

INRA, UMR1260 Nutrition, Obesity and Risk of Thrombosis, Marseille, France.

出版信息

J Nutr. 2013 Apr;143(4):448-56. doi: 10.3945/jn.112.172734. Epub 2013 Feb 20.

Abstract

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.

摘要

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。

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