scholarly journals Endothelial dysfunction and arterial abnormalities in childhood obesity

2006 ◽  
Vol 30 (7) ◽  
pp. 1041-1049 ◽  
Author(s):  
M R Skilton ◽  
D S Celermajer
Keyword(s):  
Childhood Obesity ◽  
Endothelial Dysfunction

scholarly journals Urinary Biomarkers of Inflammation and Oxidative Stress Are Elevated in Obese Children and Correlate with a Marker of Endothelial Dysfunction

2019 ◽  
Vol 2019 ◽  
pp. 1-10 ◽  
Author(s):  
Vaithinathan Selvaraju ◽  
Priscilla Ayine ◽  
Moni Fadamiro ◽  
Jeganathan Ramesh Babu ◽  
Michael Brown ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Childhood Obesity ◽  
Endothelial Dysfunction ◽  
Urine Samples ◽  
Low Grade ◽  
Oxidative Stress Markers ◽  
Obese Children ◽  
Stress Markers ◽  
Oxidative Markers ◽  
And Oxidative Stress

Obesity is a state of chronic low-level inflammation closely associated with oxidative stress. Childhood obesity is associated with endothelial dysfunction, inflammation, and oxidative stress markers individually. This study was aimed at determining the association between the biomarkers of inflammation, oxidative stress, and endothelial dysfunction in urine samples of healthy, overweight, and obese children. Eighty-eight elementary school children aged between 6 and 10 years participated in this study. Anthropometric measurements were measured using WHO recommendations. The biomarkers of low-grade inflammation such as C-reactive protein (CRP), interleukin-6 (IL-6), and α-1-acid glycoprotein (AGP); oxidative stress markers such as 8-isoprostane and 8-hydroxy-2′-deoxyguanosine (8-OHdG); and endothelin-1 (ET-1) were analyzed in urine samples. The area under the curve (AUC) by the receiver operating characteristics (ROC) was analyzed to identify the best urinary biomarker in childhood obesity. Linear regression and Pearson correlation were analyzed to determine the association between the parameters. The obese participants have significantly increased levels of CRP, AGP, IL-6, and 8-isoprostane compared to normal-weight participants. The overweight participants had significantly increased levels of ET-1 and 8-OHdG but not the obese group compared to the NW group. The AUC for urinary CRP (AUC: 0.847, 95% CI: 0.765-0.930; p<0.0001) and 8-isoprostane (AUC: 0.857, 95% CI: 0.783-0.932; p<0.0001) showed a greater area under ROC curves compared to other inflammatory and oxidative markers. The urinary CRP and 8-isoprostane significantly correlated with the obesity measures (body mass index, waist circumference, and waist-to- height ratio) and ET-1, inflammatory, and oxidative markers. The increased urinary inflammatory markers and 8-isoprostane can serve as a noninvasive benchmark for early detection of the risk of developing cardiovascular disease.

Elevated Circulating Tissue Factor Procoagulant Activity, Factor VII, Plasminogen Activator Inhibitor-1 and VCAM-1 in Childhood Obesity: Evidence of a Procoagulant State and Endothelial Dysfunction?,

Blood ◽  
2011 ◽  
Vol 118 (21) ◽  
pp. 3338-3338
Author(s):  
Anamika Singh ◽  
Jay Gunawardana ◽  
Tara Alexis McCoy ◽  
Tina Nguyen ◽  
Stephanie Vander Veur ◽  
...  
Keyword(s):  
Childhood Obesity ◽  
Endothelial Dysfunction ◽  
Tissue Factor ◽  
Plasminogen Activator ◽  
Plasminogen Activator Inhibitor ◽  
Obese Group ◽  
Healthy Weight ◽  
Obese Children ◽  
Activator Inhibitor ◽  
Pai 1

Abstract Abstract 3338 Childhood obesity is increasing in prevalence and associated with risk of type 2 diabetes (T2DM) and coronary disease. Adult obesity and T2DM are associated with alterations in the coagulation and fibrinolytic systems. Tissue Factor (TF) is the principal initiator of blood coagulation and is both prothrombotic and proinflammatory. In mouse models of obesity, TF and plasminogen activator inhibitor (PAI)-1 genes are upregulated. We tested the hypothesis that childhood obesity is associated with elevated levels of circulating TF and markers of coagulation, fibrinolysis, and endothelial dysfunction. Forty-seven children were recruited and classified based on Body Mass Index (BMI) percentile (CDC growth curves) as underweight (≤5th percentile; n=1), healthy weight (>5–84.9th percentile; n=22), overweight (≥85%-94.9th percentile; n=3) and obese (≥95th percentile; n=21). We compared the findings in 21 obese children (10.1±1.5 years, mean age ± SD) and 22 healthy weight children (9.9±1.6 years). Circulating membrane bound TF procoagulant activity (TF-PCA), measured in whole blood lysates by a two-stage clotting assay (Key et al, Blood;1998:91), was elevated in obese compared to healthy weight children (60.6±32.5 vs 34.0±13.5 U/ml, mean ± SD, p=0.005). TF-PCA levels in obese children were comparable to levels observed by us in adults with T2DM (69.5±11.5; n=18). Plasma factor (F) VIIC (1.00±0.20 vs 0.90±0.20 U/ml; p=0.03) was elevated in obese group. Plasma FVIIa, FVIII, TF antigen, fibrinogen, and thrombin-antithrombin III, and microparticles (MP) were not different between groups. In fibrinolytic system, plasma PAI-1 was elevated in obese group (37.3±18.0 vs 25.6±15.0 ng/ml; p=0.03), and tissue plasminogen activator (tPA) antigen (6.7±3.4 vs 5.1±2.0 ng/ml, p=0.07) showed a similar trend. Endothelial markers, soluble vascular cell adhesion molecule-1 (sVCAM-1; 709.2±444.5 vs 526.5±184.8 ng/ml; p=0.05) and von-Willebrand Factor (VWF; 1057.4±139.8 vs 987.9±130.8 mU/ml; p=0.07) showed a trend towards higher levels in obesity, suggesting endothelial dysfunction. BMI correlated with circulating TF-PCA (r=0.36; p=0.01), FVIIC (r=0.36; p=0.01), and PAI-1 (r=0.38; p=0.009). TF-PCA correlated with sVCAM-1 (r=0.36; p=0.01), suggesting a potential endothelial contribution to the circulating TF-PCA. Plasma FVIIa (r=−0.29; p=0.053) appeared to be inversely related to TF-PCA possibly related to removal of FVIIa from plasma by binding to membrane TF. There was an inverse relationship between MP and FVIII (r= −0.42; p=0.004) and VWF (r=−0.37; p=0.01), which may reflect binding of FVIII and vWF to microparticles. Conclusions: Obesity, even in children, causes a potential procoagulant state characterized by increased circulating TF-PCA, FVIIC and PAI-1, and is associated with evidence suggesting endothelial dysfunction. Elevated levels of endothelial markers have been shown to predict development of T2DM, and elevated FVIIC has been associated with carotid intima-media thickness in young adults. Overall, these alterations may be basis for the increased risk of cardiovascular disease now documented in childhood obesity as well. Larger studies are needed to define the effect of childhood obesity on the hemostatic systems and the impact of intervention with weight reduction on the observed changes. Disclosures: No relevant conflicts of interest to declare.

scholarly journals Assessment of Endothelial Dysfunction in Childhood Obesity and Clinical Use

2013 ◽  
Vol 2013 ◽  
pp. 1-19 ◽  
Author(s):  
Luc Bruyndonckx ◽  
Vicky Y. Hoymans ◽  
Amaryllis H. Van Craenenbroeck ◽  
Dirk K. Vissers ◽  
Christiaan J. Vrints ◽  
...  
Keyword(s):  
Childhood Obesity ◽  
Endothelial Dysfunction ◽  
Cardiovascular Complications ◽  
Endothelial Damage ◽  
Western Society ◽  
Noncommunicable Diseases ◽  
Novel Biomarkers ◽  
Endothelial Integrity

The association of obesity with noncommunicable diseases, such as cardiovascular complications and diabetes, is considered a major threat to the management of health care worldwide. Epidemiological findings show that childhood obesity is rapidly rising in Western society, as well as in developing countries. This pandemic is not without consequences and can affect the risk of future cardiovascular disease in these children. Childhood obesity is associated with endothelial dysfunction, the first yet still reversible step towards atherosclerosis. Advanced research techniques have added further insight on how childhood obesity and associated comorbidities lead to endothelial dysfunction. Techniques used to measure endothelial function were further brought to perfection, and novel biomarkers, including endothelial progenitor cells, were discovered. The aim of this paper is to provide a critical overview on bothin vivoas well asin vitromarkers for endothelial integrity. Additionally, an in-depth description of the mechanisms that disrupt the delicate balance between endothelial damage and repair will be given. Finally, the effects of lifestyle interventions and pharmacotherapy on endothelial dysfunction will be reviewed.

scholarly journals Childhood obesity–related endothelial dysfunction: an update on pathophysiological mechanisms and diagnostic advancements

2016 ◽  
Vol 79 (6) ◽  
pp. 831-837 ◽  
Author(s):  
Luc Bruyndonckx ◽  
Vicky Y Hoymans ◽  
Katrien Lemmens ◽  
José Ramet ◽  
Christiaan J Vrints
Keyword(s):  
Childhood Obesity ◽  
Endothelial Dysfunction ◽  
Pathophysiological Mechanisms

Clinical aspects of reactive oxygen and nitrogen species

2004 ◽  
Vol 71 ◽  
pp. 121-133 ◽  
Author(s):  
Ascan Warnholtz ◽  
Maria Wendt ◽  
Michael August ◽  
Thomas Münzel
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Risk Factor ◽  
Endothelial Dysfunction ◽  
Vascular Tissue ◽  
Rapid Development ◽  
Reactive Oxygen ◽  
Clinical Aspects ◽  
No Production ◽  
Oxygen Species

Endothelial dysfunction in the setting of cardiovascular risk factors, such as hypercholesterolaemia, hypertension, diabetes mellitus and chronic smoking, as well as in the setting of heart failure, has been shown to be at least partly dependent on the production of reactive oxygen species in endothelial and/or smooth muscle cells and the adventitia, and the subsequent decrease in vascular bioavailability of NO. Superoxide-producing enzymes involved in increased oxidative stress within vascular tissue include NAD(P)H-oxidase, xanthine oxidase and endothelial nitric oxide synthase in an uncoupled state. Recent studies indicate that endothelial dysfunction of peripheral and coronary resistance and conductance vessels represents a strong and independent risk factor for future cardiovascular events. Ways to reduce endothelial dysfunction include risk-factor modification and treatment with substances that have been shown to reduce oxidative stress and, simultaneously, to stimulate endothelial NO production, such as inhibitors of angiotensin-converting enzyme or the statins. In contrast, in conditions where increased production of reactive oxygen species, such as superoxide, in vascular tissue is established, treatment with NO, e.g. via administration of nitroglycerin, results in a rapid development of endothelial dysfunction, which may worsen the prognosis in patients with established coronary artery disease.

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