adenosine diphosphate/obesity

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Leptin does not play a major role in platelet aggregation in obesity and leptin deficiency.

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OBJECTIVE A recent study suggested that high concentrations of leptin enhance platelet aggregations. Therefore, the aim of this study was to investigate whether platelet aggregation is altered in patients with leptin gene mutations compared with obese subjects or controls. METHODS Four men (one

Obesity and antiplatelet effects of acetylsalicylic acid and clopidogrel in patients with stable angina pectoris after percutaneous coronary intervention.

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BACKGROUND Obesity is a cluster of medical conditions affecting several pathophysiological processes, including platelet (PLT) function. OBJECTIVE We evaluated the association between obesity and PLT response to dual antiplatelet therapy over 1 month in patients with stable angina pectoris after

Obesity is associated with poor response to clopidogrel and an increased susceptibility to protease activated receptor-1 mediated platelet activation.

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Obesity is associated with a prothrombotic state resulting from increased thrombin generation, platelet hyper-reactivity, and decreased fibrinolysis. Data on the influence of obesity on clopidogrel-mediated platelet inhibition are conflicting and limited to platelet function tests. Moreover, there

Comparison of cationic propyl gallate and adenosine diphosphate for the measurement of aspirin effectivity with optical aggregometry.

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To compare the newer inductor of platelet aggregation cationic propyl gallate (CPG) with adenosine diphosphate (ADP) for the examination of aspirin (ASA) effectivity with optical aggregometry. In total,116 patients were prospectively enrolled with a stable cardiovascular disease, taking ASA 100

Obesity is associated with impaired platelet-inhibitory effect of acetylsalicylic acid in nondiabetic subjects.

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OBJECTIVE Platelet aggregation responses to acetylsalicylic acid (ASA) show considerable interindividual variation, the causes of which are largely unknown. We determined whether variation in insulin action is associated with that of ASA on platelets. METHODS In all, 10 nonobese (age 50+/-3 y, BMI

Platelet Functions are Decreased in Obesity and Restored after Weight Loss: Evidence for a Role of the SERCA3-Dependent ADP Secretion Pathway.

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In obesity, platelets are described as hyperactive, mainly based on increased platelet size and presence of pro-thrombotic plasmatic molecules. We explored platelet functions, including calcium signalling in obesity, and the effect of weight loss. We included 40 obese patients (women with body mass

Effect of exercise training and weight loss on platelet reactivity in overweight patients with coronary artery disease.

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OBJECTIVE Obesity is associated with increased platelet reactivity. Greater platelet reactivity presages adverse events in patients with coronary artery disease (CAD). We investigated whether exercise training and weight loss reduce platelet reactivity in overweight subjects with CAD. METHODS Study

Effect of obesity and serum leptin level on clopidogrel resistance.

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OBJECTIVE Clopidogrel inhibits platelet aggregation by blockade of platelet adenosine diphosphate (ADP) P2Y12 receptor. Leptin is the obesity gene product, and its serum level increases with obesity. Platelets have leptin receptors on their surfaces. Hyperleptinemia may induce ADP-mediated platelet

Platelet aggregation in obese and diabetic subjects: association with leptin level.

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To clarify the relationship between serum leptin concentration and platelet aggregation mechanism, we investigated serum leptin concentration and agonist-induced platelet aggregation in eight obese subjects and eight non-obese and non-diabetic controls. In addition we also measured them in 15 type 2

Impaired resting muscle energetics studied by (31)P-NMR in diet-induced obese rats.

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OBJECTIVE Mitochondrial activity is altered in skeletal muscle of obese, insulin-resistant or type 2 diabetic patients. We hypothesized that this situation was associated with profound adaptations in resting muscle energetics. For that purpose, we used in vivo (31)P-nuclear magnetic resonance

Clopidogrel resistance response in patients with coronary artery disease and metabolic syndrome: the role of hyperglycemia and obesity.

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BACKGROUND Despite the proven benefits of clopidogrel combined aspirin therapy for coronary artery disease (CAD), CAD patients with metabolic syndrome (MS) still tend to have coronary thrombotic events. We aimed to investigate the influence of metabolic risk factors on the efficacy of clopidogrel

Morbid obesity and metabolic syndrome in Ossabaw miniature swine are associated with increased platelet reactivity.

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BACKGROUND Metabolic syndrome (MetS) and type 2 diabetes mellitus in humans are associated with increased platelet activation and hyperreactivity of platelets to various agonists. Ossabaw swine develop all the hallmarks of MetS including obesity, insulin resistance, hypertension, dyslipidemia,

Effect of obesity on platelet reactivity and response to low-dose aspirin.

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Insufficient platelet function suppression by aspirin is a predictor of cardiovascular events in high-risk patients. The authors assessed the impact of obesity on platelet responsiveness before and after 2 weeks of aspirin 81 mg/d in 2014 people. Obese individuals had greater baseline platelet

Reduction of inflammatory cytokine concentrations and improvement of endothelial functions in obese women after weight loss over one year.

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BACKGROUND Visceral fat is a key regulator site for the process of inflammation, and atherosclerotic lesions are essentially an inflammatory response. RESULTS Fifty-six healthy premenopausal obese women (age range 25 to 44 years, body mass index 37.2+/-2.2, waist to hip ratio range 0.78 to 0.92) and

Absence of leptin resistance in platelets from morbidly obese individuals may contribute to the increased thrombosis risk in obesity.

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Clinical studies have shown that elevated leptin levels are an independent cardiovascular risk factor. However, little is known about the existence of platelet resistance to leptin in the setting of obesity. We examined the effects of leptin on platelet aggregation in morbidly obese subjects (n =

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