Vitamin E is a group of isomers that includes α-, β-, γ- and δ-tocopherol and α-, β-, γ- and δ-tocotrienol. Tocopherols and tocotrienols are important fat soluble antioxidants in humans. Both α-tocopherol and γ-tocopherol are present in the diet in larger quantities than all of the other isomers. Most trials looking at the effects of vitamin E on cardiovascular disease have used the α-tocopherol isomer. The α-tocopherol isomer is also the most common form found in dietary supplements. Some studies have shown a beneficial effect of α-tocopherol on cardiovascular disease, but other studies have reported negative results. Relatively little is known about how increases in levels of one isomer affects the levels of the other isomers and how this may relate to health benefits or disease. However, supplementation with α-tocopherol has been shown to decrease plasma levels of γ-tocopherol.
To investigate the effects of different forms of vitamin E on cellular and serum tocopherol concentrations as well as excretion of urinary tocopherol metabolites, investigators1 fed 58 subjects with type 2 diabetes either 500 mg of α-tocopherol, 500 mg of a mixed tocopherol compound containing 60 % γ-tocopherol, or a placebo. The researchers measured the serum, erythrocyte and platelet, as well as urinary tocopherol metabolite concentrations at baseline and again at 6 weeks. The results showed that serum tocopherol concentrations increased with both treatments. Serum and cellular γ-tocopherol levels increased significantly (4-fold) in the mixed tocopherol group, but fell significantly in the α-tocopherol group. In addition, significant increases in excretion of the tocopherol metabolites α-carboxyethyl-hydroxychroman (α-CEHC) and γ-CEHC were detected after supplementation with α-tocopherol and γ-tocopherol, respectively. Urinary γ-CEHC also increased after supplementation with α-tocopherol.
These results suggest that high dose supplementation with α-tocopherol causes a doubling of α-tocopherol levels in cells and serum but causes a reduction in levels of γ-tocopherol. Studies show that low levels of γ-tocopherol are found in patients with coronary artery disease, but these subjects have normal levels of α-tocopherol. Supplementation with high doses of γ-tocopherol increased serum level of α-tocopherol and also caused a 4-fold increase in erythrocyte, cellular, serum and platelet levels of γ-tocopherol. Tocopherols are metabolised by cytochrome P450 mediated oxidation followed by ω-oxidation in the liver. Supplementation with α-tocopherol caused an increase in the excretion of γ-CEHC as well as a decrease in plasma and red blood cell levels of γ-tocopherol. This suggests that the decrease in cellular γ-tocopherol was because of increased metabolism to γ-CEHC, which may reflect the displacement of γ-tocopherol by α-tocopherol in lipoproteins in the liver.
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