Metabolic syndrome as a prothrombogenic state

Berkovskaya, M A; Бутрова, С А

doi:10.14341/2071-8713-5239

Cited by 2 publications

(2 citation statements)

References 35 publications

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“…Strong positive correlation between blood platelet count and the number of present MetS components was documented upon adjustment for a variety of biosocial factors (age, smoking, alcohol use, and physical activity). Therefore, thrombocytosis can partially explain the augmented cardiovascular risk in MetS patients (Muratova, 2004 ; Berkovskaya and Butrova, 2009 ).…”

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confidence: 99%

Platelet hemostasis in patients with metabolic syndrome and type 2 diabetes mellitus: cGMP- and NO-dependent mechanisms in the insulin-mediated platelet aggregation

et al. 2015

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Patients with metabolic syndrome (MetS) and type 2 diabetes mellitus (T2DM) have high risk of microcirculation complications and microangiopathies. An increase in thrombogenic risk is associated with platelet hyperaggregation, hypercoagulation, and hyperfibrinolysis. Factors leading to platelet activation in MetS and T2DM comprise insulin resistance, hyperglycemia, non-enzymatic glycosylation, oxidative stress, and inflammation. This review discusses the role of nitric oxide (NO) in the regulation of platelet adhesion and aggregation processes. NO is synthesized both in endotheliocytes, smooth muscle cells, macrophages, and platelets. Modification of platelet NO-synthase (NOS) activity in MetS patients can play a central role in the manifestation of platelet hyperactivation. Metabolic changes, accompanying T2DM, can lead to an abnormal NOS expression and activity in platelets. Hyperhomocysteinemia, often accompanying T2DM, is a risk factor for cardiovascular accidents. Homocysteine can reduce NO production by platelets. This review provides data on the insulin effects in platelets. Decrease in a number and sensitivity of the insulin receptors on platelets in T2DM can cause platelet hyperactivation. Various intracellular mechanisms of anti-aggregating insulin effects are discussed. Anti-aggregating effects of insulin are mediated by a NO-induced elevation of cGMP and upregulation of cAMP- and cGMP-dependent pathways. The review presents data suggesting an ability of platelets to synthesize humoral factors stimulating thrombogenesis and inflammation. Proinflammatory cytokines are considered as markers of T2DM and cardiovascular complications and are involved in the development of dyslipidemia and insulin resistance. The article provides an evaluation of NO-mediated signaling pathway in the effects of cytokines on platelet aggregation. The effects of the proinflammatory cytokines on functional activity of platelets are demonstrated.

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confidence: 99%

Platelet hemostasis in patients with metabolic syndrome and type 2 diabetes mellitus: cGMP- and NO-dependent mechanisms in the insulin-mediated platelet aggregation

et al. 2015

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“…It is known that metabolic syndrome, in particular, such components as obesity and insulin resistance, are closely associated with the disorders in the systems of coagulation and fibrinolysis, which leads to the increase in the risk of the development of cardiovascular diseases (Berkovskaya and Butrova, 2009). In patients with obesity, the hyperactivity of thrombocytes, as the main component of metabolic syndrome, is a pathogenetic factor of atherotrombogenesis, which is manifested as an increased adhesion and a capability to aggregate.…”

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confidence: 99%

ASSOCIATION OF THE DELETION ALLELE OF THE INSERTION/DELETION POLYMORPHISM OF αIIbβ3 INTEGRIN GENE AND METABOLIC SYNDROME IN YOUNG NORTHERNERS

Корнеева¹,

Воевода²,

Семаев³

et al. 2019

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The rationale for the present study is explained by a high spread of metabolic syndrome among the young population, living in an area equivalent to the Far North. The study is aimed at the investigation of the association between a deletion allele of the polymorphism of deletion/insertion in the αIIbβ3 integrin gene and metabolic syndrome in young residents Khanty-Mansiysk Autonomous Okrug – Ugra (Russia). The 758 young people aged 18-44 (mean age 36.62±5.12 years old) with metabolic syndrome and 77 healthy young people without metabolic disorders were examined. The carriership of the allele I associated with the cardiovascular risk was revealed in 63% of the examined patients that had an increased risk of the development of metabolic disorders (OR 1.409, 95% CI 0.858-2.311, p=0.253). There was no significant difference between the native and non-native populations in the rate of occurrence of allele I (62.2% and 64.7%). Genotype II had significant association with arterial hypertension (OR 1.377, 95 % CI 0.912-2.080, p=0.073), obesity (OR 1.353, 95% CI 0.825-2.219, p=0.071), hypercholesterinemia (OR 1.386, 95% CI 0.977-1.966, p=0.115), hypertriglyceridemia (OR 1.232, 95% CI 0.889-1.706, p=0.097). It was established that the non-native population had a higher risk of the development of abdominal obesity, arterial hypertension, and hypercholesterinemia, unlike the native population that had a significantly higher risk of the development of triglyceridemia. The materials of the article can be useful for the evaluation of genetic predisposition to myocardial infarction, stroke, and thromboembolism, which will allow for timely indication of preventive measures.

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Metabolic syndrome as a prothrombogenic state

Cited by 2 publications

References 35 publications

Platelet hemostasis in patients with metabolic syndrome and type 2 diabetes mellitus: cGMP- and NO-dependent mechanisms in the insulin-mediated platelet aggregation

Platelet hemostasis in patients with metabolic syndrome and type 2 diabetes mellitus: cGMP- and NO-dependent mechanisms in the insulin-mediated platelet aggregation

ASSOCIATION OF THE DELETION ALLELE OF THE INSERTION/DELETION POLYMORPHISM OF αIIbβ3 INTEGRIN GENE AND METABOLIC SYNDROME IN YOUNG NORTHERNERS

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