Cluster‐determinant 36 (CD36) impacts on vitamin E postprandial response. Issue 12 (2nd October 2014)

• Record Type: Journal Article
• Authors: Goncalves, Aurélie; Roi, Stéphanie; Nowicki, Marion; Niot, Isabelle; Reboul, Emmanuelle
• Is Part Of: Molecular nutrition & food research. Volume 58:Issue 12(2014:Dec.)
• Page Start: 2297
• Page End: 2306
• Publication Date: 2014-10-02
• Subjects: Food -- Biotechnology -- Periodicals; Food -- Microbiology -- Periodicals; Nutrition -- Periodicals; Food -- Toxicology -- Periodicals; Nutrition -- Periodicals; Food Microbiology -- Periodicals; Food Technology -- Periodicals; Molecular Biology -- Periodicals; 664.0705
• DOI: 10.1002/mnfr.201400339
• Languages: English
• ISSNs: 1613-4125

Abstract

<abstract abstract-type="main"> <title> <x xml:space="preserve">Abstract</x> </title> <sec id="mnfr2264-sec-0010" sec-type="section"> <title>Scope</title> <p>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.</p> </sec> <sec id="mnfr2264-sec-0020" sec-type="section"> <title>Methods and results</title> <p>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.</p> </sec> <sec id="mnfr2264-sec-0030" sec-type="section"> <title>Conclusion</title> <p>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.</p> </sec> </abstract>