Impaired insulin-induced platelet antiaggregating effect in obesity and in obese NIDDM patients

Trovati, Mariella; Mularoni, E.; Burzacca, S.; Ponziani, M. C.; Massucco, Paola; Mattiello, Luigi; Piretto, Valentina; Cavalot, Franco; Anfossi, Giovanni

doi:10.2337/diabetes.44.11.1318

Cited by 58 publications

(60 citation statements)

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“…22,[28][29][30] Under physiological conditions, insulin is known to decrease platelet aggregability through reduction of platelet responses to ADP and thrombin. 31,32 Platelets from insulin-resistant subjects have reduced sensitivity to the antiaggregating effects of insulin, 33 and it can be Metabolic syndrome and platelet response to leptin F Corica et al hypothesized that a greater insulin resistance in patients with a more pronounced abdominal adiposity may contribute to the profile of platelet responsiveness to leptin in our study. Dyslipidemia can also contribute to increase platelet activation.…”

Section: Discussionmentioning

confidence: 64%

Relationship between metabolic syndrome and platelet responsiveness to leptin in overweight and obese patients

et al. 2006

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Objective: To verify whether platelet responsiveness to leptin is associated with metabolic syndrome risk factors. Design: Cross-sectional study. Subjects: We studied 169 consecutive patients, mean age ¼ 43.679.9 years, with overweight (N ¼ 57) or obesity (N ¼ 112). Measurements: Cluster analysis was used to generate three clusters based on platelet responsiveness to increasing doses of leptin. Profiles of metabolic syndrome risk factors of the three clusters were compared by discriminant analysis. Results: Platelet responsiveness to leptin was absent in cluster 1, whereas cluster 3 had the greatest platelet aggregation response to leptin pre-incubation. Plasma leptin levels significantly decreased from cluster 1 to cluster 3 in both gender. Patients in cluster 2 had an intermediate profile of leptin responsiveness. Highest body mass index (BMI) values were more frequent in non-responders, whereas the prevalence of high waist circumference, as well as hypertriglyceridemia and hypertension, increased with increasing responsiveness to leptin from cluster 1 to cluster 3. Pattern of metabolic syndrome risk factors qualified as group specific in 69.0% of the cluster 1, 54.9% of the cluster 2 and 55.8% of the cluster 3. Circulating leptin, waist circumference, plasma triglycerides and BMI defined distinctive patterns of metabolic syndrome risk factors in the clusters. Conclusions: In overweight and obese outpatients, metabolic syndrome risk factors parallel to some extent platelet responsiveness to leptin. Such a correlation involves plasma leptin levels, waist circumference, plasma triglycerides and BMI, and may contribute to the excess risk of cardiovascular events in overweight and obese patients.

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Section: Discussionmentioning

confidence: 64%

Relationship between metabolic syndrome and platelet responsiveness to leptin in overweight and obese patients

et al. 2006

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“…Impaired myocardial glucose utilization is therefore unlikely to be a primary defect predisposing non-diabetic individuals or patients with NIDDM for the development of CHD. This does not dispute a role for insulin resistance per se in being a risk factor for cardiovascular disease but suggests that the mechanisms linking the two phenomena are likely to be indirect or could involve some other insulin sensitive process(es) such as resistance to the platelet antiaggregating effect of insulin, which also characterizes patients with NIDDM [32].…”

Section: Discussionmentioning

confidence: 99%

Insulin resistance characterizes glucose uptake in skeletal muscle but not in the heart in NIDDM

et al. 1998

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Signs or symptoms of macrovascular disease are frequently found even prior to the development of noninsulin-dependent diabetes mellitus (NIDDM) [1]. This suggests that coronary heart disease (CHD) and NIDDM share a pathophysiologic feature, which predisposes to both diseases. Classic risk factors such as serum cholesterol, age, gender, hypertension and smoking explain only a fraction of the 2±4-fold increase in cardiovascular mortality in patients with NIDDM [1,2]. Insulin resistance, usually measured by quantitating the rate of insulin-stimulated glucose uptake, qualifies as the underlying pathophysiologic abnormality for both CHD and NIDDM, since it predicts, independent of other risk factors, both disorders [3,4].The mechanisms linking insulin resistance to CHD are unclear but could involve lipid abnormalities such as an increase in the concentration of atherogenic small dense LDL particles, which accompanies insu- Diabetologia (1998) Summary Skeletal muscle insulin resistance and coronary heart disease (CHD) often precede non-insulin-dependent diabetes mellitus (NIDDM). A recent study showed the myocardium of patients with CHD to be insulin resistant, independent of blood flow. We determined whether myocardial insulin resistance is a feature of NIDDM patients with no CHD. Skeletal muscle and myocardial glucose uptake were determined in 10 patients with NIDDM and 9 ageand weight-matched normal men of similar age and body mass index men using [18 F]-2-fluoro-2-deoxy-dglucose and positron emission tomography under normoglycaemic hyperinsulinaemic conditions. Whole body glucose uptake, as determined by the euglycaemic clamp technique, was significantly lower in the patients with NIDDM (35 ± 3 mmol/kg body weight´min) than the normal subjects (45 ± 3 mmol/ kg body weight´min, p < 0.02). Insulin-stimulated femoral muscle glucose uptake was significantly lower in the patients with NIDDM (71 ± 6 mmol/kg muscle´min) than in the normal subjects (96 ± 5 mmol/ kg muscle´min, p < 0.01). Whole body glucose uptake was correlated with femoral muscle glucose uptake in the entire group (r = 0.76, p < 0.001), in patients with NIDDM and in normal subjects. Rates of insulin-stimulated myocardial glucose uptake were comparable between the patients with NIDDM (814 ± 76 mmol/kg muscle´min) and the normal subjects (731 ± 63 mmol/kg muscle´min, p > 0.4). Whole body or femoral muscle, and myocardial glucose uptake were not correlated in all subjects, patients with NIDDM or normal subjects. We conclude that insulin resistance of the myocardium is not a feature of uncomplicated NIDDM. [Diabetologia (1998) 41: 555-559] Keywords Myocardium, insulin resistance, non-insulin-dependent diabetes mellitus, positron emission tomography.

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“…Several clues indicate that IGT or Type II diabetes represent a prothrombotic state due to a dysbalance between procoagulant and antithrombotic factors and between activators and inhibitors of plasminogen activation. Insulin resistance typical of IGT and Type II diabetes might contribute to this dysbalance [65,66]. In our study, stenosis higher than 40 % was found to predominantly originate from atherothrombosis [39,40] and to rest on a risk profile including almost exclusively factors directly or indirectly related to coagulation and fibrinolysis: fibrinogen, antithrombin III (higher concentrations being protective), Lp(a), factor V Leiden mutation, smoking, alcohol intake (protective if mild) ( Table 5).…”

Section: Discussionmentioning

confidence: 99%

Impaired glucose tolerance, Type II diabetes mellitus and carotid atherosclerosis: prospective results from the Bruneck Study

et al. 2000

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Atherosclerotic vascular diseases such as myocardial infarction, stroke and lower extremity arteriopathy are well-known severe complications of impaired glucose tolerance (IGT) and Type II (non-insulin-dependent) diabetes mellitus [1±7] and account for up to 60±70 % of deaths in diabetic subjects [8]. Impaired glucose tolerance and Type II diabetic patients often have, however, multiple metabolic, haemodynamic and haemocoagulative defects such as high triglycerides and low HDL cholesterol, high blood pressure and high fibrinogen [9±15], which are cardiovascular risk factors in themselves [16]. These defects can precede the development of glucose intolerance by several years [17, 18]. Thus, the independent contribution of glucose intolerance and its bio- Diabetologia (2000) Abstracts Aims/hypothesis. Cardiovascular disease is a wellknown severe complication of impaired glucose tolerance and Type II (non-insulin-dependent) diabetes mellitus. The independent contribution of glucose intolerance to cardiovascular disease and the underlying pathogenic mechanisms are still, however, not clear. Methods. In this prospective population-based study, 826 subjects aged 40±79 years underwent high resolution duplex ultrasound examinations of carotid arteries and extensive clinical and laboratory screenings for potential vascular risk factors at baseline and 5 years later. The ultrasound protocol involved measurements of maximum axial diameter of atherosclerotic plaques, if any, in common and internal carotid arteries on both sides and enable differentiation of two main stages in carotid artery disease, termed early non-stenotic and advanced stenotic atherosclerosis. Intima-media thickness was assessed at the follow-up examination. Results. Type II diabetes and, to a lesser extent, impaired glucose tolerance were found to be statistically significant risk predictors of 5-year changes in carotid atherosclerosis. These associations were in part independent of other vascular risk factors typically clustering with glucose intolerance. Both impaired glucose tolerance and Type II diabetes mellitus were not independently related to early non-stenotic atherosclerosis. In contrast, Type II diabetes mellitus was the strongest single risk predictor of advanced stenotic atherosclerosis [odds ratio 5.0 (95 % confidence intervals 2.3±11.1)] and impaired glucose tolerance was of relevance as well [odds ratio 2.8 (1.2±6.4)] (p < 0.001). Conclusion/interpretation. Impaired glucose tolerance and, to a greater extent, Type II diabetes were strong independent predictors of advanced carotid atherosclerosis in our prospective population-based study. [Diabetologia (2000) 43: 156±164]

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Impaired insulin-induced platelet antiaggregating effect in obesity and in obese NIDDM patients

Cited by 58 publications

References 0 publications

Relationship between metabolic syndrome and platelet responsiveness to leptin in overweight and obese patients

Relationship between metabolic syndrome and platelet responsiveness to leptin in overweight and obese patients

Insulin resistance characterizes glucose uptake in skeletal muscle but not in the heart in NIDDM

Impaired glucose tolerance, Type II diabetes mellitus and carotid atherosclerosis: prospective results from the Bruneck Study

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