Abstract

Abdominal obesity and metabolic syndrome are important risk factors of atherothrombosis. In obesity, metabolic and inflammatory-mediated tissular injury could contribute to enhanced shedding of procoagulant microparticles (MPs). At sites of endothelium injury, the swift recruitment of procoagulant-MPs enables the initiation of blood coagulation and thrombus growth. In obese female, we sought to evaluate the impact of vey low caloric diet (VLCD) on procoagulant MPs levels, fibrinolytic status, inflammation and endothelium damage. Circulating biomarkers of vascular damage, fibrinolytic status, platelet activation, inflammation were measured before, 30 and 90 days after VLCD. Microparticles were measured by flow cytometry and capture assays. Their procoagulant abilities were quantified by functional prothrombinase assay and their cellular origin were determined (endothelium, platelet, leukocyte, lymphocyte and erythrocyte phenotypes). 24 obese females (39 ± 10 yr) were prospectively enrolled. At baseline, higher PAI-l or platelet-derived procoagulant MPs levels were respectively evidenced in patients with metabolic syndrome or insulin resistance (HOMA>2.4). Procoagulant leukocytes-derived MPs were associated with waist circumference at baseline (r = 0.534: p = 0.010) and at 90 days follow-up (r = 0.487; p = 0.021). At 90 days, weight reduction (−9.8%) was associated with a lowering of blood pressure, improvement of metabolic parameters and a significant reduction of PAI-1 (−38%), procoagulant platelet-derived MPs (−43%) and leptin (−32%) levels. In obese female, very low caloric diet enables an overall improvement of the haemostatic balance characterized by the reduction of PAI-levels, a fibrinolysis inhibitor, diminished platelet release of procoagulant MPs and reduction of leptin levels, an adipocyte-derived cytokine.

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