title: Pathophysiological Role of Adiponectin, Leptin and Asymmetric Dimethylarginine in the Process of Atherosclerosis.
abstract: 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.
authors.affiliation: Section of Endocrinology, Second Department of Internal Diseases, Faculty of Medicine, Medical University of Plovdiv, Plovdiv,
  Bulgaria|Clinic of Endocrinology, St. George University Hospital, Plovdiv, Bulgaria
authors.forename: Daniela Iv
authors.initials: DI
authors.lastname: Koleva
authors.affiliation: Section of Endocrinology, Second Department of Internal Diseases, Faculty of Medicine, Medical University of Plovdiv, Plovdiv,
  Bulgaria|Clinic of Endocrinology, St. George University Hospital, Plovdiv, Bulgaria
authors.forename: Maria M
authors.initials: MM
authors.lastname: Orbetzova
authors.affiliation: Department of Physiology, Faculty of Medicine, Medical University of Plovdiv, Plovdiv, Bulgaria
authors.forename: Julia G
authors.initials: JG
authors.lastname: Nikolova
authors.affiliation: Department of Clinical Laboratory, Faculty of Pharmacy, Medical University of Plovdiv, Plovdiv, Bulgaria|Clinical Laboratory, St. George University Hospital, Plovdiv, Bulgaria
authors.forename: Tanya I
authors.initials: TI
authors.lastname: Deneva
mesh_terms: D052242:Adiponectin / Q000276:immunology / Q000378:metabolism*; D001120:Arginine / Q000031:analogs & derivatives* / Q000276:immunology / Q000378:metabolism; D050197:Atherosclerosis / Q000276:immunology / Q000378:metabolism*; D002097:C-Reactive Protein / Q000276:immunology; D019040:E-Selectin / Q000378:metabolism; D019332:Endothelin-1 / Q000378:metabolism; D006801:Humans; D018799:Intercellular Adhesion Molecule-1 / Q000378:metabolism; D016209:Interleukin-8 / Q000276:immunology; D020738:Leptin / Q000276:immunology / Q000378:metabolism*; D009569:Nitric Oxide / Q000378:metabolism; D014409:Tumor Necrosis Factor-alpha / Q000276:immunology; D019010:Vascular Cell Adhesion Molecule-1 / Q000378:metabolism
chemical_list: D052242:Adiponectin; D019040:E-Selectin; D019332:Endothelin-1; D016209:Interleukin-8; D020738:Leptin; D014409:Tumor Necrosis Factor-alpha; D019010:Vascular Cell Adhesion Molecule-1; D018799:Intercellular Adhesion Molecule-1; D009569:Nitric Oxide; C018524:N,N-dimethylarginine; D002097:C-Reactive Protein; D001120:Arginine