UT Southwestern study shows vitamin E works as anti-inflammatory agent in type II diabetes

July 10, 2000

DALLAS -- July 11, 2000 - A high intake of vitamin E can help reduce heart disease and stroke risk in type II diabetics, UT Southwestern researchers have found.

In a study published in the July 11 issue of Circulation, Drs. Ishwarlal Jialal and Sridevi Devaraj found that increased inflammation caused by white blood cells -- monocytes -- was reduced when diabetics were given 1,200 International Units per day of natural vitamin E (alpha-tocopherol) for three months.

"This is the first study that shows that vitamin E has anti-inflammatory effects in diabetic patients," said Jialal, professor of pathology and internal medicine. "It could be a further therapy to prevent vascular complications in diabetes since inflammation seems to be critical as a causative factor in diabetic vascular disease.''

The main cause of death and morbidity in type II diabetes, also known as non-insulin dependent diabetes mellitus, are vascular complications. Previous studies by Jialal, the principal investigator in this study and a senior investigator in the Center for Human Nutrition, have shown that vitamin E is a potent antioxidant.

Type II diabetics with and without macrovascular disease were compared with nondiabetics.

Twenty-five participants in each of the three groups were given 1,200 IU of vitamin E daily for three months followed by two-months without the supplement. Blood was taken from all the patients at the beginning of the study, after three months and again after the washout. The effect of the vitamin E was similar in all three groups.

The study showed that type II diabetic patients have increased inflammation, as shown by the activity of a pivotal cell (the circulating monocyte) in plaque formation on artery walls.

The monocyte is a crucial and the most readily accessible cell involved in atherogenesis.

Study data showed that the diabetic monocyte was more active and promoted more inflammation and more free radicals and cytokines, or messenger molecules. The diabetic monocyte also caused more adhesion to the lining cells of the artery wall.

"It was very important to elucidate the pivotal role for inflammation in diabetic vascular disease and examine how it could be modulated," said Devaraj, assistant professor in the clinical biochemistry and human metabolism division in the Department of Pathology.
-end-
The American Diabetes Association funded the study.




UT Southwestern Medical Center

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