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Mol Nutr Food Res. 2014 Dec;58(12):2297-306. doi: 10.1002/mnfr.201400339. Epub 2014 Oct 2.

Cluster-determinant 36 (CD36) impacts on vitamin E postprandial response.

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INRA, UMR 1260, Nutrition, Obesity and Risk of Thrombosis, Marseille, France; INSERM, UMR 1062, Marseille, France; Aix-Marseille Université, Marseille, France.



A single nucleotide polymorphism in the cluster determinant 36 (CD36) gene has recently been associated with plasma α-tocopherol concentration, suggesting a possible role of this protein in vitamin E intestinal absorption or tissue uptake.


To investigate the involvement of CD36 in vitamin E transport, we first evaluated the effect of CD36 on α- and γ-tocopherol transmembrane uptake and efflux using transfected HEK cells. γ-Tocopherol postprandial response was then assessed in CD36-deficient mice compared with wild-type mice, after the mice had been fully characterized for their α-tocopherol, vitamin A and lipid plasma, and tissue contents. Both α- and γ-tocopherol uptake was significantly increased in cells overexpressing CD36 compared with control cells. Compared with wild-type mice, CD36-deficient mice displayed a significantly decreased cholesterol hepatic concentration, and males exhibited significantly higher triacylglycerol contents in liver, brain, heart, and muscle. Although tissue α-tocopherol concentration after adjustment for lipid content was not modified, γ-tocopherol postprandial response was significantly increased in CD36-deficient mice compared with controls, likely reflecting the postprandial hypertriglyceridemia observed in these mice.


Our findings show for the first time that CD36 participates-directly or indirectly-in vitamin E uptake, and that CD36 effect on postprandial lipid metabolism in turn modifies vitamin E postprandial response.


Bioavailability; CD36; Intestinal absorption; Transgenic mice; α-Tocopherol; γ-Tocopherol

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