Open AccessPathophysiological Role of Adiponectin, Leptin and Asymmetric Dimethylarginine in the Process of Atherosclerosis
Author(s) -
Daniela Iv. Koleva,
Maria Orbetzova,
Julia Nikolova,
Tanya Deneva
Publication year - 2016
Publication title -
folia medica/folia medica
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.245
H-Index - 21
eISSN - 1314-2143
pISSN - 0204-8043
DOI - 10.1515/folmed-2016-0039
Subject(s) - proinflammatory cytokine , adiponectin , medicine , endothelial dysfunction , endocrinology , leptin , insulin resistance , asymmetric dimethylarginine , adipose tissue , inflammation , nitric oxide , insulin , biology , obesity , arginine , biochemistry , amino acid
Adipose tissue is recognized as a rich source of proinflammatory mediators that may directly contribute to vascular injury, insulin resistance, and atherogenesis. Many studies have shown that adiponectin has antiatherogenic and anti-inflammatory properties. Adiponectin acts not only as a factor increasing insulin sensitivity, and the protective effect may result from its ability to suppress production of proinflammatory cytokines. It negatively regulates the expression of TNF-alpha and C-reactive protein (CRP) in adipose tissue; reduces expression of vascular and intracellular adhesion molecules (VCAM-1, ICAM-1), E-selectin, interleukin-8 (IL-8). Hyperleptinemia has been linked with the development of hypertension and endothelial dysfunction/atherosclerosis, two main pathophysiological conditions associated with cardiovascular disease development. Leptin-mediated increases in sympathetic nervous system activity may be among the principal mechanisms evoking obesity related hypertension. Leptin stimulates the secretion of proinflammatory cytokines, and increases the release of endothelin-1 (ET-1), which may promote hypertension. Increased serum levels of asymmetric dimethylarginine (ADMA), a physiological regulator of the biosynthesis of nitric oxide (NO), promote the process of atherosclerosis, leading to the occurrence of endothelial dysfunction and cardiovascular disease.