Vitamin E Absorption and Digestion

How the Digestion and Absorption of Vitamin E Takes Place

The absorption of vitamin E takes place in the jejunum of the small intestine by passive diffusion in the presence of bile and dietary fat. Micelles synthesis is also required. After circulating in chylomicrons, Vitamin E is transported via the lymph and bloodstream to the liver, where it is incorporated into very low-density lipoproteins (VLDLs) to be delivered to the body’s tissues. However, tocopherol is also broken down into low density and high-density lipoproteins. More than 90% of excess vitamin E is stored in adipose tissue in a non-esterified form.
Absorption effectiveness for vitamin E varies considerably between one individual and another, with a range of 20% to 70%. Very high intake of the vitamin apparently reduces the absorption rate. However, absorption is improved in the presence of dietary lipids.
Tocopherols exist freely in foods in a form in which they can be absorbed. However, the tocotrienols, which are esterified, need to be hydrolyzed before they can be absorbed. The same is true of synthetic ester forms of tocopherol. Some vitamin E can also be absorbed through the skin when applied topically as an ointment or oil.
The uptake of vitamin E by the cell can occur either by LDLs delivering vitamin E into the cell or by their release from chylomicrons and VLDLs with the help of lipoprotein lipase (LP). Within the cell, transportation of tocopherol depends on the presence of tocopherol-binding protein (TBP). In non-adipose tissue, vitamin E is found almost exclusively in the cell membranes, from where it can be easily mobilized.

Transportation, and Metabolism

Within the enterocyte, absorbed tocopherols are incorporated into chylomicrons to be transported first through the lymph and then into circulation. Vitamin E in the form of absorbed tocopherols and tocotrienols that are not taken up by the body’s tissues are transmitted via chylomicron remnants to the liver. Some of this vitamin E is subsequently incorporated into VLDLs and secreted back into the bloodstream to be transported again to various body tissues. However, for this process to take place, an alpha-tocopherol transfer protein must be produced in the liver. When this doesn’t happen due to a genetic defect, a vitamin E deficiency can result.
Furthermore, the alpha-tocopherol transfer protein only facilitates the re-secretion of alpha-tocopherol into the blood, not other forms of vitamin E. Alpha-tocopherol is the primary form of vitamin E in the blood. The normal concentration of alpha-tocopherol (bound to lipoproteins) in the plasma is between 5 and 20 ug/ml.
Uptake of alpha-tocopherol into the cells can occur in the following ways:  
  • As receptor-mediated uptake of LDLs
  • Through lipoprotein lipase-mediated hydrolysis of chylomicrons and VLDLs
  • Through HDL-mediated nutrient delivery
The transfer of vitamin E from lipoproteins to the cell membranes might be facilitated by a phospholipid transfer protein. Within the cell, Vitamin E binds to tocopherol-binding proteins for transport. Another protein called ATP-binding cassette (ABC) is believed to facilitate transport of vitamin E outside of the cells.


Vitamin E, like the other fat-soluble vitamins, can be stored in the body for future use. More than 90% of the excess vitamin E that remains in storage can be found in adipose tissue in a non-esterified form. Besides adipose tissue, smaller amounts of vitamin E are taken up by various other body tissues, including the liver, lungs, heart, muscles, adrenal glands, spleen, and brain. However, vitamin E is not stored in the body as efficiently as the other fat-soluble vitamins, A, D, and K. Increased ingestion of vitamin E does not increase the concentration of the vitamin in these tissues appreciably. More than half of the excess amount not stored in the body’s adipose tissues and, to a lesser extent, in the heart, muscles, testes or uterus, and adrenal and pituitary glands, or circulating in the blood, is lost in the feces.
The amount of vitamin E that will be stored in the body is in direct proportion to the amount of vitamin E consumed. When intake is low, stored vitamin E in the liver, plasma, and skeletal muscles serves as a ready source for an extra supply of the vitamin where needed. However, the release of vitamin E from storage is a slow process.


Vitamin E is oxidized into the biologically inactive form tocopherol quinone, of which glucuronic acid conjugates are secreted into the bile. The major route of excretion is through the feces; a very small amount of vitamin E is also excreted in the urine.