PMID: 11926895Apr 3, 2002Paper

Effect of leptin on arterial thrombosis following vascular injury in mice

JAMA : the Journal of the American Medical Association
Peter F BodaryDaniel T Eitzman

Abstract

Complications of atherosclerosis are the leading cause of morbidity and mortality in industrialized societies. Obesity has emerged as an independent risk factor for complications of atherosclerotic vascular disease. Leptin, a hormone produced by the adipocyte, increases with obesity and appears to modulate energy balance and food intake. In addition, other actions of leptin have been proposed, including an in vitro effect on platelet aggregation. Thus, the elevated plasma leptin levels in obese individuals may promote vascular thrombosis. To test the hypothesis that leptin contributes to in vivo thrombosis via the leptin receptor. Between September 2000 and September 2001, a vascular thrombosis model was used to test male 10- to 12-week-old mice completely deficient in leptin or the leptin receptor and mice with platelet leptin-receptor deficiency. Time to formation of an occlusive thrombus in the common carotid artery following experimentally induced endothelial injury. Following onset of vascular injury, wild-type mice (n = 8) formed occlusive thrombosis in a mean (SD) of 42.2 (4.6) minutes, whereas leptin-deficient (n = 5) and leptin receptor-deficient mice (n = 7) formed occlusive thrombosis in 75.2 (10.1) and 68.6 (10.3) m...Continue Reading

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