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Biotech / Medical : Regeneron Pharmaceuticals -- Ignore unavailable to you. Want to Upgrade?

To: Miljenko Zuanic who wrote (594)	11/19/2001 6:46:54 PM
From: Miljenko Zuanic	Read Replies (1) \| Respond to of 3559

JCI Online J Clin Invest, November 2001, Volume 108, Number 10, 1533-1540 Copyright ©2001 by the American Society for Clinical Investigation -------------------------------------------------------------------------------- Article Leptin-dependent platelet aggregation and arterial thrombosis suggests a mechanism for atherothrombotic disease in obesity Stavros Konstantinides, Katrin Schäfer, Stefan Koschnick and David J. Loskutoff Department of Vascular Biology, The Scripps Research Institute, La Jolla, California, USA Address correspondence to: David J. Loskutoff, Department of Vascular Biology, The Scripps Research Institute, 10550 North Torrey Pines Road (VB3), La Jolla, California 92037, USA. Phone: (858) 784-7125; Fax: (858) 784-7353; E-mail: loskutof@scripps.edu. Received for publication April 27, 2001, and accepted in revised form September 24, 2001. Obesity is associated with increased cardiovascular morbidity and mortality and with elevated circulating levels of the satiety factor leptin. This study provides evidence for a direct link between leptin and the risk for thrombotic complications in obese individuals. For example, although arterial injury provokes thrombosis in both lean and obese (ob/ob) mice, the time to complete thrombotic occlusion is significantly delayed in the ob/ob mice, and the thrombi formed are unstable and frequently embolize. The ob/ob mice lack leptin, and intraperitoneal administration of leptin to these mice before injury restores the phenotype of lean mice by shortening the time to occlusion, stabilizing the thrombi, and decreasing the patency rate. The thrombi that form when leptin receptor-deficient obese (db/db) mice are injured also are unstable. However, in this instance, leptin has no effect. Platelets express the leptin receptor, and leptin potentiates the aggregation of platelets from ob/ob but not db/db mice in response to known agonists. These results reveal a novel receptor-dependent effect of leptin on platelet function and hemostasis and provide new insights into the molecular basis of cardiovascular complications in obese individuals. The results suggest that these prothrombotic properties should be considered when developing therapeutic strategies based on leptin.