Abstract
Vitamin E status in the body is regulated through absorptive and metabolic systems. In the liver, α-tocopherol transfer protein (αTTP) preferably binds transported α-tocopherol and transfers it to vessels. In contrast, a large part of γ-tocopherol transported into the liver is metabolized. This discrimination of vitamin E by αTTP in the liver develops in the infant period and maintains α-tocopherol/γ-tocopherol ratio in the serum at a constant level thereafter. The expression of αTTP in the liver is also changed in diabetic animals and nutritional vitamin E status, such as deficiency and sufficiency. Another major mechanism to regulate vitamin E status in the serum is the metabolism of excessive α-tocopherol to α-CEHC (2,5,7,8-tetramethyl-2-(2'-carboxyethyl)-6-hydrochroman) in the liver and the resulting α-CEHC is secreted into the urine. A large part of γ-tocopherol administered to humans at a large dose is also metabolized to γ-CEHC in the liver and the resulting γ-CEHC stimulates the secretion of sodium to the urine in the kidney. This metabolism of α-tocopherol and γ-tocopherol to α-CEHC and γ-CEHC, respectively, also contributes to the maintenance of vitamin E status in the serum.
