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Cardiac Stent Patients With Diabetes May Benefit From Drug That Counteracts Effects Of Leptin

Dec. 17, 2008 — The naturally high levels of leptin in diabetic patients may reduce the effectiveness of drug-eluting stents used to treat heart blockages, but using a chemical that differs from the one commonly used to coat stents could counteract this effect.


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The work by researchers at Columbia University Medical Center could potentially improve outcomes in diabetics who get stents, they say. Though drug-eluting stents reduce the chance coronary arteries will become blocked again, clogged stents are still more common in diabetic patients than in the general population. About 250,000 Americans with diabetes receive drug-eluting stents every year.

A hormone commonly associated with obesity – leptin – may be partly responsible, according to recently published research in the Proceedings of the National Academy of Sciences by Andrew Marks, M.D., chair of physiology & cellular biophysics and Clyde and Helen Wu Professor of Molecular Cardiology, and Steven Marx, M.D., associate professor of medicine and pharmacology. The study found that leptin, at the elevated concentrations frequently found in patients with diabetes, stimulates the growth of cells responsible for clogging the stents in mice, even in the presence of sirolimus, a drug used in many stents to prevent cell growth.

The same mouse study also identified a drug – a PI3kinase inhibitor – that counteracts the effect of leptin on cell growth. If added to current drug-eluting stents, such a drug may further reduce reclogging rates in patients with diabetes to the single digit rates seen in other patients. An improved stent could significantly reduce the numbers of patients who eventually need coronary bypass surgery after their stents become severely obstructed.

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The above story is reprinted from materials provided by Columbia University Medical Center, via EurekAlert!, a service of AAAS.

Note: Materials may be edited for content and length. For further information, please contact the source cited above.


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