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Study suggests insulin may have potential to prevent thrombosis leading to heart attack and stroke

BUFFALO, N.Y. -- Insulin may interfere with the cascade of reactions that promote clot formation and platelet aggregation in heart-attack patients and may help prevent clot formation and plaque development in persons at risk of heart attack and stroke, new research by University at Buffalo endocrinologists has shown.

The researchers have demonstrated that an infusion of insulin and glucose suppresses a factor that regulates genes for two pro-inflammatory proteins that promote coagulation and clot formation in smooth muscle tissue lining blood vessels.

Results of the study appear in the March issue of the Journal of Clinical Endocrinology and Metabolism.

"Our earlier research showed for the first time that insulin exerts a significant anti-inflammatory effect on blood vessel walls, and now we have linked insulin with the mechanisms that reduce clotting factors," said Paresh Dandona, M.D., UB professor of medicine and senior author on the study.

"These new findings suggest that insulin has the potential to prevent thrombosis that leads to heart attack and stroke. It also may be useful to treat persons with those conditions through the prevention of clotting and promotion of dissolution of clots."

Dandona said the findings in this study add relevance to results from the Diabetes and Insulin-Glucose Infusion in Acute Myocardial Infarction (DIGAMI) study, conducted in Stockholm, which showed that diabetic patients experiencing an acute heart attack who received a low dose infusion of insulin and glucose had a better outcome than patients who weren't infused. "The DIGAMI study showed that insulin has a positive effect on acute myocardial infarction, but the mechanisms weren't clear," he said. "Our studies are defining the mechanisms." The current investigation targeted a pro-inflammatory transcription factor, early growth response gene-1 (Egr-1), and concentrations in blood plasma of two proteins whose expression is regulated by Egr-1 -
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Contact: Lois Baker
ljbaker@buffalo.edu
716-645-5000 x 1417
University at Buffalo
21-Mar-2002


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