scholarly journals Dyslipidemia, subclinical inflammation, hepatic cholestasis and endothelial dysfunction in schoolchildren with excess fat: A study from the United Arab Emirates

PLoS ONE ◽  
2019 ◽  
Vol 14 (1) ◽  
pp. e0210316 ◽  
Author(s):  
Elhadi H. Aburawi ◽  
Sania Al Hamad ◽  
Javed Yasin ◽  
Lolowa A. Almekhaini ◽  
Abdul-Kader Souid
Keyword(s):  
Endothelial Dysfunction ◽  
United Arab Emirates ◽  
Subclinical Inflammation

scholarly journals Subclinical Inflammation and Endothelial Dysfunction in Young Patients with Diabetes: A Study from United Arab Emirates

PLoS ONE ◽  
2016 ◽  
Vol 11 (7) ◽  
pp. e0159808 ◽  
Author(s):  
Elhadi H. Aburawi ◽  
Juma AlKaabi ◽  
Taoufik Zoubeidi ◽  
Abdullah Shehab ◽  
Nader Lessan ◽  
...  
Keyword(s):  
Endothelial Dysfunction ◽  
United Arab Emirates ◽  
Young Patients ◽  
Subclinical Inflammation ◽  
Patients With Diabetes

scholarly journals Association between functional neurometry test results and blood biomarkers indicative of anaemia, subclinical inflammation, and endothelial dysfunction

2021 ◽  
Vol 14 (5) ◽  
pp. 225-233
Author(s):  
Renata de Melo Guerra Ribas ◽  
Valdenilson Ribeiro Ribas ◽  
Diélita Carla Lopes de Oliveira ◽  
Marcelo Tavares Viana ◽  
Joyce Gomes de Moraes ◽  
...  
Keyword(s):  
Endothelial Dysfunction ◽  
Subclinical Inflammation ◽  
Test Results ◽  
Blood Biomarkers

scholarly journals Subclinical Inflammation and Endothelial Dysfunction in Patients with Chronic Pancreatitis and Newly Diagnosed Pancreatic Cancer

2015 ◽  
Vol 61 (4) ◽  
pp. 1121-1129 ◽  
Author(s):  
A. Gasiorowska ◽  
R. Talar-Wojnarowska ◽  
A. Kaczka ◽  
A. Borkowska ◽  
L. Czupryniak ◽  
...  
Keyword(s):  
Pancreatic Cancer ◽  
Chronic Pancreatitis ◽  
Endothelial Dysfunction ◽  
Subclinical Inflammation ◽  
Newly Diagnosed

scholarly journals Adipocytokines in metabolically healthy obesity

2019 ◽  
Vol 13 (3) ◽  
pp. 169-175
Author(s):  
Sofia G. Shulkina ◽  
Elena N. Smirnova ◽  
Maxim I. Yudin ◽  
Mikhail A. Osadchuk ◽  
Maxim V. Trushin
Keyword(s):  
Insulin Resistance ◽  
Blood Pressure ◽  
Endothelial Dysfunction ◽  
Metabolic Disorders ◽  
International Diabetes Federation ◽  
Resistance Index ◽  
High Density Lipoproteins ◽  
Control Group ◽  
Subclinical Inflammation ◽  
Tnf Α

The aim of the investigation was to study the relationship among adipokines, markers of subclinical inflammation and endothelial dysfunction in patients with metabolic healthy obesity (MHO). The study included 50 persons aged 25-50 years with obesity in the absence of metabolic disorders (International Diabetes Federation criteria, 2005, marked as MHO), the control group consisted of 50 healthy respondents without obesity. We studied clinical and biochemical parameters, insulin resistance index (HOMA-IR), levels of leptin, soluble leptin receptors (sLR), resistin, adiponectin, C-reactive protein (CRP-hs), tumor necrosis factor-alpha (TNF-α), interleukin-6 (IL-6), vascular endothelial growth factor (VEGF), endothelin-1 (ET-1), von Willebrand factor, free leptin index was calculated in a formula (FLI = leptin × 100 / sLR). In MHO patients, independently of HOMA-IR index, there was an increase in leptin, FLI, resistin, VEGF, and IL-6 parameters. The concentration of CRP-hs and TNF-α in MHO group with HOMA-IR ≥2.7 was increased. Systolic blood pressure correlated with leptin level (r=0.43, P<0.05), FLI (r=0.54; P=0.01), TNF-α (r=0.44; P<0.05) and IL-6 (r=0.33; P<0.05); diastolic blood pressure - with leptin level (r=0.35, P<0.05). Links between high density lipoproteins and leptin (r=–0.55 and r=–0.60; P<0.01), resistin (r=0.32; P<0.05 and r=0.60; P<0.01) and VEGF (r=–0.70, P<0.01) were established. The VEGF level correlated with HOMA-IR (r=0.62; P<0.01), leptin (r=0.29; P<0.05), FLI (r=0.50; P<0.05), resistin (r=0.70; P<0.01), IL-6 (r=0.74, P<0.01) and ET-1 (r=0.29; P<0.05). Obese patients without metabolic disorders, having normotension and normal insulin sensitivity, are less influenced to adverse cardiovascular risks due to less expressed hormonal and inflammatory activation of adipose tissue and, as a result, less pronounced endothelial dysfunction. While insulin resistance develops, cardiovascular risk increases due to activation of subclinical inflammation, angiogenic endothelial dysfunction and leptin resistance.

scholarly journals Subclinical Inflammation, Endothelial Progenitor Cell Depletion, and Endothelial Dysfunction in Adolescents with Obesity

2009 ◽  
Vol 23 (S1) ◽  
Author(s):  
Hong Huang ◽  
Judith A. Groner ◽  
Jennifer Kuck ◽  
Lisa Nicholson ◽  
Robert Murray ◽  
...  
Keyword(s):  
Endothelial Dysfunction ◽  
Endothelial Progenitor Cell ◽  
Progenitor Cell ◽  
Cell Depletion ◽  
Subclinical Inflammation ◽  
Endothelial Progenitor

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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