Bile salts and dietary lipids play critical roles in the absorption of vitamin E and their esters into intestinal epithelial cells through micellization. Pancreatic lipases facilitate the micellization of vitamin E as a consequence of hydrolysis of non-vitamin E lipids by forming mixed micells. The vitamin E esters (e.g., «-tocopherol acetate), on the other hand, require hydrolysis by the pancreatic lipases prior to micel-lization and uptake into the enterocytes. The uptake of vitamin E from the mixed micells is thought to be a passive diffusion process; however, the role of a scavenger receptor class B type I (SR-BI) has also been suggested.
The intracellular trafficking of vitamin E may involve its incorporation into chylomicrons. Both a- and y-tocopherols are equally incorporated into chylomicrons, which are then secreted into the lymphatic system. An ATP-binding cassette, subfamily A, member 1 (ABCA1) transport protein-directed efflux of vitamin E from epithelial cells into HDL followed by direct transport into the portal vein has also been suggested as an important alternative pathway for vitamin E absorption. Dietary fats increase chylomicron-mediated absorption while a low-fat diet increases HDL-mediated absorption of vitamin E.89 The absence of dietary fat results in little absorption of vitamin E.90 Despite a low-fat diet, high bioavailability was reported when vitamin E was added with emulsifier onto fortified breakfast cereal, suggestive of micellization as a critical factor for its absorption.91 No apparent differences in intestinal absorption of various forms of vitamin E (e.g., a- and y-tocopherols or RRR- and SRR-a-tocopherols) have been observed.92 Overall, 20% to 80% of vitamin E is absorbed from the intestinal lumen into the bloodstream. The liver is an important storage site. y-Tocopherol is secreted primarily into the bile while a-tocopherol enters the circulation, where it is found in much higher levels than y-tocopherol, even though the latter predominates in the diet. This difference is attributed to a liver cytosolic binding protein, «-tocopherol transfer protein (a-TTP) that is selective for a-tocopherol.
The tocopherols in lymph are associated with chylomi-crons and VLDLs. Circulating tocopherols are also carried by a-TTP, which preferentially incorporates them into blood low-density lipoproteins (LDLs). The tocopherols are readily and reversibly bound to most tissues, including adipose tissue, and the vitamin is thus stored. The vitamin is concentrated in membrane structures, such as mitochondria, endoplasmic reticulum, and nuclear and plasma membranes.
Although "Simon metabolites" (tocopheronic acid and its y-lactone) were first identified as the primary vitamin E metabolites by in vitro sample oxidation, the biologically relevant are the 2-carboxyethyl-6-hydroxychroman (CEHC) products (Fig. 28.12). Thus «-, ¡-, y-, and <5-CEHCs are identified as metabolites of the respective tocopherols. The terminal methyl group is oxidized to a carboxylic acid and shortened by several steps of ¡-oxidation to produce CEHC. The CEHC metabolites undergo glucuronide and sulfate conjugations, and most of the CEHC metabolites are found in urine as these conjugates. These metabolites are also excreted in the bile and vitamin E may undergo some entero-hepatic circulation.92
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