מתוך אתר medicontext.co.il
WESTPORT, CT (Reuters Health) – Insulin produces changes in inflammatory mediators that may reduce the risk of atherosclerosis, according to researchers from the State University of New York at Buffalo.
Findings from prior studies have tied insulin resistance to atherogenesis and have also shown that the insulin-sensitizing drug troglitazone has anti-inflammatory effects. In the current study, the SUNY researchers investigated whether insulin itself has anti-inflammatory effects.
Dr. Paresh Dandona and colleagues tested the anti-inflammatory hypothesis by administering insulin- and non-insulin-containing intravenous solutions to 10 obese, nondiabetic subjects. Blood samples were taken prior to infusion and at 2, 4, and 6 hours after infusion, the team reports in The Journal of Clinical Endocrinology and Metabolism for July.
The investigators found that insulin reduced concentrations of the pro-inflammatory compound nuclear factor kappa-B (NF kappa-B) and increased concentrations of the compound that inhibits NF kappa-B. In addition, insulin reduced reactive oxygen species generation by mononuclear cells and produced a reduction in the levels of several other pro-inflammatory mediators.
"This is a brand-new property of insulin," Dr. Dandona noted in a SUNY statement. "Since atherosclerosis is the result of an inflammation of the vessel wall, we believe insulin will prove to be anti-atherosclerotic in the long run."
"At the very least, these results should indicate to physicians that they should not be reluctant to prescribe insulin when it is indicated for fear that it may increase the risk of heart attack," he added.
J Clin Endocrinol Metab 2001;86:3257-3265.
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