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Supplemental alpha-tocopherol (AT) given to type 2 diabetic patients decreases monocyte activity and soluble cell adhesion molecules, thereby possibly reducing the risk of macrovascular disease in this group, according to researchers.
Researchers studied 25 subjects with type 2 diabetes who had no vascular complications and 25 subjects with type 2 diabetes who had macrovascular complications, along with 25 age- and sex-matched healthy controls.
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All the subjects received 1,200 IU of natural alpha-tocopherol per day for 3 months.
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Vitamin E therapy significantly decreased LDL oxidizability in all three groups.
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Both diabetic groups showed a significant decrease in soluble cell adhesion molecules compared with the controls.
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Among the diabetics, monocytes released significantly more superoxide anion and interleukin-1-beta and had greater adhesion to endothelium than control subjects.
Researchers assert that their study has two main findings. One is that it is the first demonstration that there is increased inflammation in diabetes, whether patients have heart disease or not. "This was manifested by the monocyte plaque formation and the production of more superoxide, more cytokines and messenger molecules which bound to the endothelium," one of the researchers explained.
"The second important finding, which is totally novel," said one researcher, "is that when we gave the subjects vitamin E there was a substantial reduction in the monocyte function. Obviously we showed an antioxidant effect, as we have shown in other studies, but in addition, we showed that vitamin E, in high doses, is an anti-inflammatory agent."
"What we are saying is that heart disease and stroke risk can be lowered because vitamin E reduces plaque formation. I am suggesting that this is adjunctive therapy in diabetes that would add to reduction in cardiovascular events."
Researchers also speculated that "vitamin E might also have an effect on the metabolic syndrome that causes diabetes and might act to prevent the disease."
Circulation July 11, 2000:102:191-196.
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