The association between obesity and blood clots is well known; but the cause has remained a mystery. Now, new research with mice conducted by scientists at the University of Michigan Medical School and published in the April 3 issue of the Journal of the American Medical Association, indicates that leptin may be responsible.

Our results suggest that clot formation begins with some type of interaction between leptin and the leptin receptor on platelets blood cells which stick together to make clots, says Daniel T. Eitzman, M.D., a cardiologist at the U-M Cardiovascular Center and an assistant professor of internal medicine in the Medical School.

Knowing how to block this leptin-receptor interaction could help prevent heart attacks and strokes in people who are either obese or overweight, which is half the adult population of the United States.

According to Eitzman, leptin released by fat cells regulates body weight in part by suppressing appetite. When leptin levels in blood go up, the brain signals us to stop eating. But the system breaks down for those who are grossly overweight. Since they have more and larger leptin-producing fat cells than thinner people, their leptin levels increase substantially with every pound of additional weight gain. When leptin reaches very high levels in the blood, Eitzman explains, obese people become resistant to leptins signal making them increasingly vulnerable to leptin-induced blood clotting.

While it certainly plays a major role, Eitzman emphasizes that leptin may not be the only factor involved. The link between obesity and cardiovascular disease is very complex, and there is much we dont know about how other blood clotting factors are regulated in o
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Contact: Sally Pobojewski
pobo@umich.edu
734-615-6912
University of Michigan Health System
2-Apr-2002