Effects of serum homocysteine and adiponectin levels on platelet aggregation in untreated patients with essential hypertension

Ekmekçi, Hakan; Ekmekçi, Özlem Balcı; Erdine, Serap; Sönmez, Hüseyin; Ataev, Yusup; Öztürk, Zeynep; Bütün, İlknur; Gürel, Çiğdem Bayram; Kuçur, Mine; Turfaner, Nurver; Ulutin, Turgut; Pürisa, Sevim; Vural, Vural Ali

doi:10.1007/s11239-008-0292-0

Cited by 12 publications

(15 citation statements)

References 41 publications

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“…Second, omentin has been shown to increase insulin sensitivity [28] . Rodrigues et al [29] (1) 60.61±15.02 (1) 59.81±9.88 (1) 0.5663 Men (%) 90 (70.87) (2) 15 (53.57) (2) 38 (73.08) (2) 0.1548 BMI (kg/m 2 ) 25.52±3.35 (1) 24.71±3.74 (1) 25.73±3.14 (1) 0.4171 Smoking (%) 54 (42.52) (2) 9 (32.14)…”

Section: Discussionmentioning

confidence: 95%

“…14 (26.92) (2) 0.1227 Family history (%) 25 (19.69) (2) 7 (25.00) (2) 9 (17.31) (2) 0.7114 SBP (mmHg) 135.00 (33.00) …”

Section: Discussionmentioning

confidence: 99%

“…These adipokines play important roles in carbohydrate and lipid metabolism, homeostasis, insulin resistance, diabetes, atherosclerosis, vascular endothelial dysfunction, inflammation, and cardiovascular function [2][3][4][5][6] . Omentin, a recently identified fat deposition-specific adipokine codified by two genes (1 and 2), is highly and selectively expressed in visceral omental adipose tissue [7] .…”

Section: Introductionmentioning

confidence: 99%

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Association of serum omentin-1 levels with coronary artery disease

et al. 2011

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Aim: Omentin-1, a novel adipokine expressed in visceral adipose tissue, is negatively correlated with insulin resistance and obesity. Decreased omentin-1 expression has been found in many chronic inflammatory diseases. However, the role of omentin-1 in coronary artery disease (CAD) has not been elucidated. The aim of the present study was to determine whether serum concentration of omentin-1 was independently associated with CAD. Methods: One hundred and fifty five patients with CAD were divided into two groups: acute coronary syndrome (ACS) and stable angina pectoris (SAP). A total of 52 healthy participants served as controls. Serum concentrations of omentin-1 and interleukin-6 (IL-6) were measured using ELISA. The association of omentin-1 with CAD and cardiovascular disease risk factors was evaluated. Results: Serum omentin-1 levels were lower in patients with ACS or SAP compared with controls (ACS, 113.08±61.43 ng/mL; SAP, 155.41±66.89 ng/mL; control, 254.00±72.9 ng/mL; P<0.01). Patients with ACS also had lower serum concentrations of omentin-1 compared with patients with SAP (P<0.01). Serum concentration of omentin-1 was negatively correlated with body mass index (r=-0.17, P<0.05) and serum IL-6 concentration (r=-0.19, P<0.05). Furthermore, multiple logistic regression analysis showed that serum omentin-1 concentrations were independently correlated with CAD. Conclusion: The findings suggest that serum concentrations of omentin-1 are related to CAD.

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Section: Discussionmentioning

confidence: 95%

“…14 (26.92) (2) 0.1227 Family history (%) 25 (19.69) (2) 7 (25.00) (2) 9 (17.31) (2) 0.7114 SBP (mmHg) 135.00 (33.00) …”

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Association of serum omentin-1 levels with coronary artery disease

et al. 2011

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“…In addition to its metabolic actions, adiponectin has anti-inflammatory and antiatherogenic effects through its receptors (AdipoR1 and AdipoR2) expressed on monocytes, smooth muscle cells, and endothelial cells. Furthermore, there are investigations that confer an antithrombotic role on adiponectin (10) and associate platelet activation with low serum adiponectin (4). The aims of the present work were 1) to compare platelet aggregation and sCD40L levels in patients with MS and evaluate its association with adiponectin concentrations and 2) to study the in vitro effects of adiponectin on platelet aggregation and sCD40L release.…”

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confidence: 99%

Adiponectin diminishes platelet aggregation and sCD40L release. Potential role in the metabolic syndrome

Restituto¹,

Colina²,

Varo

et al. 2010

American Journal of Physiology-Endocrinology and Metabolism

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(CD40L), is increased in the metabolic syndrome (MS) and released from platelets. We hypothesized that adiponectin modulates platelet function, and we sought to evaluate the association of adiponectin and sCD40L levels with platelet aggregation in MS and the effects of adiponectin on platelet aggregation and activation. Platelet aggregation and circulating adiponectin, sCD40L and P-selectin were determined in 30 controls and 30 patients with MS. Also, in vitro studies were performed in platelet-rich plasma from nine healthy volunteers. Adiponectin receptors were demonstrated by Western blotting and flow cytometry. ADP and epinephrine platelet aggregation was measured after preincubation with adiponectin. sCD40L and P-selectin secretion was measured in the supernatants by ELISA. Patients with MS had higher sCD40L and P-selectin than controls (5.96 Ϯ 0.50 vs. 4.28 Ϯ 0.41 ng/ml, P Ͻ 0.05, and 151 Ϯ 8 vs. 122 Ϯ 9 ng/ml, P Ͻ 0.05). By contrast, adiponectin was lower in patients with MS than in controls (5.25 Ϯ 0.30 vs. 7.35 Ϯ 0.34 g/ml, P Ͻ 0.001). Higher platelet aggregation was found in MS. Adiponectin inversely correlated with P-selectin (R ϭ Ϫ0.35, P ϭ 0.009), sCD40L (r ϭ Ϫ0.24, P ϭ 0.05) and epinephrine and collagen induced aggregation (r ϭ Ϫ0.80, P ϭ 0.005; r ϭ Ϫ0.70, P ϭ 0.011). Platelets express the receptors for adiponectin. Platelet aggregatory response to epinephrine and ADP significantly decreased following preincubation with adiponectin (96 Ϯ 4 vs. 23 Ϯ 3%, P Ͻ 0.001, and 102 Ϯ 9 vs. 85 Ϯ 9%, P ϭ 0.004). Adiponectin prevented platelet sCD40L release (1.63 Ϯ 0.15 vs. 2.04 Ϯ 0.20 ng/ml, P Ͻ 0.001). Enhanced platelet aggregation and activation markers are found in MS associated with low adiponectin concentrations. Novel evidence is provided demonstrating that adiponectin has antithrombotic properties, since it inhibits platelet aggregation and platelet activation. soluble CD40 ligand; platelets; platelet activation; P-selectin THE METABOLIC MYNDROME (MS) consists of the convergence of a variety of risk factors in the same individual and is characterized by a general proinflammatory and prothrombotic state that interacts synergistically, causing or accelerating the progression of atherosclerosis. There are different definitions to describe this syndrome. Currently, the more accepted definitions are those of the National Cholesterol Education Program -Third Adult Treatment Panel (NCEP ATP III) and the World Health Organization (WHO). In both, obesity, insulin resistance, dyslipidemia, and hypertension are considered to underlie the metabolic syndrome. Prothrombosis is not yet included in any definition of MS, but the International Diabetes Federation (IDF) consensus group identifies a prothrombotic state related to MS and advises investigating the predictive power of these extra criteria for cardiovascular risk or diabetes. In fact, several investigations demonstrate the association between a prothrombotic state and diabetes (23), obesity (20), and hypertension (17).Furthermore, recent studies demonstrate th...

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“…Different biological functions have been reported for ADPN following binding with its receptors. Several studies have suggested that low plasma levels of ADPN correlate with the pathogenesis of obesity-related diseases: type 2 diabetes, hypertension and atherosclerosis (Kiris et al 2006;Ekmekçi et al 2009;Li et al 2009). …”

Section: Introductionmentioning

confidence: 99%

Adiponectin induces growth inhibition and apoptosis in cervical cancer HeLa cells

Xie

Wang

et al. 2011

Biologia

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Obesity is a known risk factor for postmenopausal cervical cancer. In human, plasma adiponectin (ADPN) levels are inversely associated with obesity. ADPN may influence the pathogenesis of cervical cancer. In this paper, the effects of ADPN on the proliferation of the cervical cancer HeLa cells and its underlying mechanism were studied. We discovered that two ADPN receptors were expressed in HeLa cells and ADPN inhibited the proliferation of HeLa cells. Western-blotting showed that ADPN activated AMP kinase in HeLa cells. Reverse transcriptase-polymerase chain reaction revealed ADPN down-regulated the expression of cell cycle regulators cyclin D1 and c-myc, and induced the expression of p21 WAF1/CIP1 and p53. These results indicate that ADPN inhibits proliferation and induces apoptosis of HeLa cells by altering the expression of cell cycle regulators.

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Effects of serum homocysteine and adiponectin levels on platelet aggregation in untreated patients with essential hypertension

Cited by 12 publications

References 41 publications

Association of serum omentin-1 levels with coronary artery disease

Association of serum omentin-1 levels with coronary artery disease

Adiponectin diminishes platelet aggregation and sCD40L release. Potential role in the metabolic syndrome

Adiponectin induces growth inhibition and apoptosis in cervical cancer HeLa cells

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