Endothelial dysfunction in patients with obesity
نویسندگان
چکیده
Endothelial dysfunction has been considered in the pathogenesis of obesity widespread population. The purpose this review was to provide updated information about pathogenetic features and markers endothelial obese patients. We mentioned systemic disorders obesity, such as oxidative stress, an increase pro-inflammatory cytokines – tumor necrosis factor alpha, interleukin-6, arginase activity. also discussed role insulin resistance development dysfunction, well product adipose tissue metabolism monocyte chemoattractant protein-1. participation perivascular tissue, hyperoxia regulation inflammation considered. illustrated influence atherogenic concentrations oxidized low-density lipoproteins, asymmetric dimethyl-L-arginine level on function. Changes laboratory parameters were analyzed: endothelin-1, levels microalbuminuria, homocysteine uric acid. described cytological (circulating vascular cells, microparticles) instrumental (endothelium-dependent vasodilation, peripheral arterial tonometry, intima-media complex thickness common carotid artery, ultrasound kidneys examination with duplex scanning renal arteries) methods for assessing Factors that risk cardiovascular complications hypertension stiffness, high lipoprotein triglycerides, reduced physical determination function patients can be important predicting pathology system. Information assessment may expand possibilities early diagnosis prevention complications.
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This article was originally published in a journal by OMICS Publishing Group, and the attached copy is provided by OMICS Publishing Group for the author’s benefit and for the benefit of the author’s institution, for commercial/research/educational use including without limitation use in instruction at your institution, sending it to specific colleagues that you know, and providing a copy to you...
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ژورنال
عنوان ژورنال: Regionarnoe krovoobra?enie i mikrocirkulâciâ
سال: 2022
ISSN: ['2712-9756', '1682-6655']
DOI: https://doi.org/10.24884/1682-6655-2022-21-3-4-11