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Am J Clin Nutr. 2014 Jul;100(1):168-75. doi: 10.3945/ajcn.114.085720. Epub 2014 May 7.

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

Author information

1
From Institut National de la Recherche Agronomique (INRA), Unité Mixte de Recherche (UMR) INRA1260, Marseille, France (PB, CD, MN, and RB); the Institut National de la Recherche Médicale (INSERM), UMR_S 1062, Marseille, France (PB, CD, MN, and RB); Aix Marseille Université, Nutrition Obésité et Risque Thrombotique, Marseille, France (PB, CD, MN, and RB); the Centre d'Investigation Clinique (CIC) Hôpital de la Conception, Marseille, France (SM); and the CIC Hôpital Nord, Marseille, France (NL).

Abstract

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 × 10(-4)) 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.

PMID:
24808487
DOI:
10.3945/ajcn.114.085720
[Indexed for MEDLINE]

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