Editing Vitamin E (section)

==Absorption, metabolism, excretion ==
Tocotrienols and tocopherols, the latter including the stereoisomers of synthetic alpha-tocopherol, are absorbed from the intestinal lumen, incorporated into [[chylomicron]]s, and secreted into the [[portal vein]], leading to the [[liver]]. Absorption efficiency is estimated at 51% to 86%,<ref name="DRItext" /> and that applies to all of the vitamin E family – there is no discrimination among the vitamin E [[vitamer]]s during absorption. Bile is necessary for chylomicron formation, so disease conditions such as [[cystic fibrosis]] result in biliary insufficiency and vitamin E malabsorption.<ref name=PKIN2020VitE/> When consumed as an alpha-tocopheryl acetate dietary supplement, absorption is promoted when consumed with a fat-containing meal.<ref name=PKIN2020VitE/> Unabsorbed vitamin E is excreted via feces. Additionally, vitamin E is excreted by the liver via [[bile]] into the intestinal lumen, where it will either be reabsorbed or excreted via feces, and all of the vitamin E vitamers are metabolized and then excreted via urine.<ref name="DRItext" /><ref name=Manolescu2008 />

Upon reaching the liver, RRR-alpha-tocopherol is preferentially taken up by [[alpha-tocopherol transfer protein]] (α-TTP). All other forms are degraded to 2'-carboxethyl-6-hydroxychromane (CEHC), a process that involves truncating the phytic tail of the molecule, then either sulfated or [[glucuronidation|glucuronidated]]. This renders the molecules water-soluble and leads to excretion via urine. Alpha-tocopherol is also degraded by the same process, to 2,5,7,8-tetramethyl-2-(2'-carboxyethyl)-6-hydroxychromane (α-CEHC), but more slowly because it is partially protected by α-TTP. Large intakes of α-tocopherol result in increased urinary α-CEHC, so this appears to be a means of disposing of excess vitamin E.<ref name="DRItext" /><ref name=Manolescu2008 />

Alpha-tocopherol transfer protein is coded by the ''TTPA'' gene on [[chromosome 8]]. The binding site for RRR-α-tocopherol is a hydrophobic pocket with a lower affinity for beta-, gamma-, or delta-tocopherols, or for the stereoisomers with an S configuration at the chiral 2 site. Tocotrienols are also a poor fit because the double bonds in the phytic tail create a rigid configuration that is a mismatch with the α-TTP pocket.<ref name=Manolescu2008 /> A rare genetic defect of the ''TTPA'' gene results in people exhibiting a progressive neurodegenerative disorder known as ataxia with vitamin E deficiency (AVED) despite consuming normal amounts of vitamin E. Large amounts of alpha-tocopherol as a dietary supplement are needed to compensate for the lack of α-TTP.<ref name=Min2007 /> The role of α-TTP is to move α-tocopherol to the plasma membrane of [[hepatocyte]]s (liver cells), where it can be incorporated into newly created very low density lipoprotein (VLDL) molecules. These convey α-tocopherol to cells in the rest of the body. As an example of a result of the preferential treatment, the US diet delivers approximately 70&nbsp;mg/d of γ-tocopherol, and plasma concentrations are on the order of 2–5 μmol/L; meanwhile, dietary α-tocopherol is about 7&nbsp;mg/d, but plasma concentrations are in the range of 11–37 μmol/L.<ref name=Manolescu2008 />

'''Affinity of α-TTP for vitamin E vitamers'''<ref name=Manolescu2008 />
{| class="wikitable"
|-
!Vitamin E compound
!Affinity
|-
|RRR-alpha-tocopherol ||100%
|-
|beta-tocopherol ||38%
|-
|gamma-tocopherol ||9%
|-
|delta-tocopherol ||2%
|-
|SSR-alpha-tocopherol ||11%
|-
|alpha-tocotrienol ||12%
|}