Genetic variants in BCMO1 and CD36 are associated with plasma lutein concentrations and macular pigment optical density in humans

Borel, Patrick; Edelenyi, Fabien Szabo de; Vincent-Baudry, Stéphanie; Malezet-Desmoulin, Christiane; Margotat, Alain; Lyan, Bernard; Gorrand, Jean-Marie; Meunier, Nathalie; Drouault-Holowacz, Sophie; Bieuvelet, Séverine

doi:10.3109/07853890.2010.531757

Cited by 85 publications

(62 citation statements)

References 56 publications

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“…Both dietary factors (17) and genetic variations between individuals (18) have been proposed to explain this phenomenon. In support of the latter factor, recent studies have shown that blood and tissue concentrations of lutein are associated with genetic polymorphisms (16,19,20).…”

Section: Introductionmentioning

confidence: 89%

“…PLS is a multivariate statistical tool often used for chemometric (38) and spectrometric modeling and has recently been applied to SNP-based predictions by our group (31) and other researchers (19,31,39,40). Because of the large number of SNPs compared with the low number of subjects and the multicollinearity between SNPs, PLS regression was chosen to identify SNPs (of the 1785 candidate SNPs) that were predictive of the postprandial chylomicron lutein response according to their variable importance in the projection (VIP) value.…”

Section: Statistics: Pls Regressionmentioning

confidence: 99%

“…Cell culture studies have shown that at least the 2 apical membrane transport proteins [ie, scavenger receptor class B type I (SR-BI) (22,23), which is encoded by SCARB1, and Niemann-Pick disease, type C1, gene-like 1 (NPC1L1) (24)] participate in the uptake of micellarized lutein. Candidate gene association studies have also suggested that other enterocyte membrane lipid transporters [ie, cluster determinant 36 (CD36) (19), ATP-binding cassette G5/G8 (ABCG5/G8) (19,20), and ATP-binding cassette subfamily member 1 (ABCA1) (16,20)] could participate in lutein absorption.…”

Section: Introductionmentioning

confidence: 99%

“…The enterocyte contains 2 enzymes that can be involved in carotenoid metabolism within the enterocyte b,b-carotene-15,15#-monooxygenase (BCMO1), which has been associated with blood lutein status (16,19,(26)(27)(28), and b,b-carotene-9,10#-oxygenase (BCO2), the involvement of which in lutein metabolism has recently been shown (29). The fraction of carotenoid that is not metabolized by these enzymes is incorporated into chylomicrons, which are secreted into the lymph and enter the bloodstream.…”

Section: Introductionmentioning

confidence: 99%

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Interindividual variability of lutein bioavailability in healthy men: characterization, genetic variants involved, and relation with fasting plasma lutein concentration

Borel¹,

Desmarchelier²,

Nowicki³

et al. 2014

The American Journal of Clinical Nutrition

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Background: Lutein accumulates in the macula and brain, where it is assumed to play physiologic roles. The bioavailability of lutein is assumed to display a high interindividual variability that has been hypothesized to be attributable, at least partly, to genetic polymorphisms. Objectives: We characterized the interindividual variability in lutein bioavailability in humans, assessed the relation between this variability and the fasting blood lutein concentration, and identified single nucleotide polymorphisms (SNPs) involved in this phenomenon. Design: In a randomized, 2-way crossover study, 39 healthy men consumed a meal that contained a lutein supplement or the same meal for which lutein was provided through a tomato puree. The lutein concentration was measured in plasma chylomicrons isolated at regular time intervals over 8 h postprandially. Multivariate statistical analyses were used to identify a combination of SNPs associated with the postprandial chylomicron lutein response (0-8-h area under the curve). A total of 1785 SNPs in 51 candidate genes were selected. Results: Postprandial chylomicron lutein responses to meals were very variable (CV of 75% and 137% for the lutein-supplement meal and the meal with tomato-sourced lutein, respectively). Postprandial chylomicron lutein responses measured after the 2 meals were positively correlated (r = 0.68, P , 0.0001) and positively correlated to the fasting plasma lutein concentration (r = 0.51, P , 0.005 for the lutein-supplement-containing meal). A significant (P = 1.9 3 10 24 )and validated partial least-squares regression model, which included 29 SNPs in 15 genes, explained most of the variance in the postprandial chylomicron lutein response. Conclusions: The ability to respond to lutein appears to be, at least in part, genetically determined. The ability is explained, in large part, by a combination of SNPs in 15 genes related to both lutein and chylomicron metabolism. Finally, our results suggest that the ability to respond to lutein and blood lutein status are related. This trial was registered at clinicaltrials.gov as NCT02100774. Am J Clin Nutr 2014;100:168-75.

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Section: Introductionmentioning

confidence: 89%

Section: Statistics: Pls Regressionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Interindividual variability of lutein bioavailability in healthy men: characterization, genetic variants involved, and relation with fasting plasma lutein concentration

Borel¹,

Desmarchelier²,

Nowicki³

et al. 2014

The American Journal of Clinical Nutrition

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“…Changes in the BCMO1 gene were associated with circulating concentrations of α and β carotenes, lycopene, lutein and zeaxanthin. These results suggest that the variation of BCMO1 gene can affect the status of carotenoids and therefore the answer to supplement [32].…”

Section: Genetic Determinants Of Carotenoids Statusmentioning

confidence: 95%

Dietary Antioxidant and Oxidative Stress: Interaction between Vitamins and Genetics

Marcadenti¹,

Lopes²,

Coelho³

2015

JNHFS

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Intakes of Lutein, Zeaxanthin, and Other Carotenoids and Age-Related Macular Degeneration During 2 Decades of Prospective Follow-up

et al. 2015

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Genetic variants in BCMO1 and CD36 are associated with plasma lutein concentrations and macular pigment optical density in humans

Abstract: these results suggest that BCMO1 and CD36 are implicated in plasma and retina concentrations of lutein and that genetic variants in these genes can modulate blood and retina concentrations of lutein.

Cited by 85 publications

References 56 publications

Interindividual variability of lutein bioavailability in healthy men: characterization, genetic variants involved, and relation with fasting plasma lutein concentration

Interindividual variability of lutein bioavailability in healthy men: characterization, genetic variants involved, and relation with fasting plasma lutein concentration

Dietary Antioxidant and Oxidative Stress: Interaction between Vitamins and Genetics

Intakes of Lutein, Zeaxanthin, and Other Carotenoids and Age-Related Macular Degeneration During 2 Decades of Prospective Follow-up

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