Vitamin E Bioavailability

Absorption and Plasma Transport

Intestinal absorption of vitamin E is dependent upon normal processes of fat absorption. Specifically, both biliary and pancreatic secretions are necessary for solubilization of vitamin E in mixed micelles containing bile acids, fatty acids, and monoglycer-ides (Figure 3). a-Tocopheryl acetates (or other esters) from vitamin E supplements are hydrolyzed by pancreatic esterases to a-tocopherol prior to absorption. Following micellar uptake by entero-cytes, vitamin E is incorporated into chylomicrons and secreted into the lymph. Once in the circulation, chylomicron triglycerides are hydrolyzed by lipopro-tein lipase. During chylomicron catabolism in the circulation, vitamin E is nonspecifically transferred both to tissues and to other circulating lipoproteins.

It is not until the vitamin E-containing chylomi-crons reach the liver that discrimination between the various dietary vitamin E forms occurs. The hepatic a-TTP preferentially facilitates secretion of «-tocopherol, specifically 2R-a-tocopherols, and not other

- Excretion

Preferential secretion

Tissue uptake of «-tocopherol

Figure 3 Intestinal vitamin E absorption and plasma lipoprotein transport. (Adapted from Traber MG (1998) Vitamin E. In: Shils ME, Olson JA, Shike M, and Ross AC (eds.) Modern Nutrition in Health and Disease, pp. 347-362. Baltimore: Williams & Wilkins.)

- Excretion

Preferential secretion

Tissue uptake of «-tocopherol

Figure 3 Intestinal vitamin E absorption and plasma lipoprotein transport. (Adapted from Traber MG (1998) Vitamin E. In: Shils ME, Olson JA, Shike M, and Ross AC (eds.) Modern Nutrition in Health and Disease, pp. 347-362. Baltimore: Williams & Wilkins.)

tocopherols or tocotrienols from the liver into the plasma in very low-density lipoproteins (VLDLs). In the circulation, VLDLs are catabolized to low-density lipoproteins (LDL are also known as the 'bad cholesterol' because high LDL levels are associated with increased risk of heart disease). During this lipolytic process, all of the circulating lipoproteins become enriched with a-tocopherol.

There is no evidence that vitamin E is transported in the plasma by a specific carrier protein, but rather it is nonspecifically transported in lipoproteins. An advantage of vitamin E transport in lipoproteins is that easily oxidizable lipids are protected by the simultaneous transport of this lipid-soluble antioxidant. Similarly, delivery of vitamin E to tissues is dependent upon lipid and lipoprotein metabolism. Thus, as per-oxidizable lipids are taken up by tissue, the tissues simultaneously acquire a lipid-soluble antioxidant.

Plasma Concentrations, Kinetics, and Tissue Delivery

Plasma a-tocopherol concentrations in normal humans range from 11 to 37 mmoll-1. When plasma lipids are taken into account the lower limits of normal are 1.6 mmol a-tocopherol/mmol lipid or 2.5 mmol a-tocopherol/mmol cholesterol. a-Tocopherol is transported in plasma lipoproteins, so if lipid concentrations are extraordinarily high or low, then correction for lipid levels are helpful to determine adequacy of vitamin E status. Additionally, a-tocopherol concentrations in erythrocytes, adipose tissue, or even peripheral nerves have been used to assess vitamin E status.

The apparent half-life of RRR-a-tocopherol in plasma of normal subjects is approximately 48 h, while that of SRR-a-tocopherol or 7-tocopherol is only 15 h.

Vitamin E is delivered to tissues by three mechanisms: transfer from triglyceride-rich lipoproteins during lipolysis; as a result of tissue lipoprotein uptake by various receptors that mediate lipoprotein uptake; and as a result of vitamin E exchange between lipoproteins or tissues. The regulation of tissue vitamin E is not well understood, but a-toco-pherol is the predominant form in tissues as a result of its dominance in plasma.

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