J. Lipid Res.
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A more recent version of this article appeared on June 1, 2006

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J. Lipid Res., doi:10.1194/jlr.M500523-JLR200
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Submitted on November 30, 2005
Revised on March 27, 2006
Accepted on March 27, 2006

Transport of vitamin E by differentiated Caco-2 cells

Kamran Anwar, Herbert J. Kayden, and M. Mahmood Hussain

Anatomy and Cell Biology, SUNY Downstate Medical Center, Brooklyn, NY 11203

Corresponding Author: mhussain{at}downstate.edu

In hepatocytes, vitamin E is secreted via the efflux pathway and is believed to associate with apoB-lipoproteins extracellularly. The molecular mechanisms involved in the uptake, intracellular trafficking, and secretion of dietary vitamin E by the intestinal cells are unknown. We observed that low concentrations of Tween-40 were better for the solubilization and delivery of vitamin E to differentiated Caco-2 cells, whereas high concentrations of Tween-40 and sera inhibited this uptake. Vitamin E uptake was initially rapid and then reached saturation. Subcellular localization revealed that vitamin E primarily accumulated in microsomal membranes. Oleic acid (OA) treatment, that induces chylomicron assembly and secretion, decreased microsomal membrane bound vitamin E in a time-dependent manner. To study secretion, differentiated Caco-2 cells were pulse labeled with vitamin E and chased in the presence and absence of OA. In the absence of OA, vitamin E was associated with intestinal high-density lipoproteins (I-HDL) whereas OA treated cells secreted vitamin E with I-HDL and chylomicrons. No extracellular transfer of vitamin E between these lipoproteins was observed. Glyburide, an antagonist of ATP cassette binding protein A1 (ABCA1), partially inhibited its secretion with I-HDL, whereas plasma HDL increased vitamin E efflux. An antagonist of microsomal triglyceride transfer protein, Brefeldin A, and monensin specifically inhibited vitamin E secretion with chylomicrons. These studies indicate that vitamin E taken up by Caco-2 cells is stored in the microsomal membranes and secreted with chylomicrons and I-HDL. Transport via I-HDL might contribute to vitamin E absorption in patients with abetalipoproteinemia receiving large oral doses of the vitamin.


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