Koleva Daniela Iv, Orbetzova Maria M, Nikolova Julia G, Deneva Tanya I
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
Folia Med (Plovdiv). 2016 Dec 1;58(4):234-240. doi: 10.1515/folmed-2016-0039.
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.
脂肪组织被认为是促炎介质的丰富来源，这些介质可能直接导致血管损伤、胰岛素抵抗和动脉粥样硬化的发生。许多研究表明，脂联素具有抗动脉粥样硬化和抗炎特性。脂联素不仅作为一种增加胰岛素敏感性的因子发挥作用，其保护作用可能源于它抑制促炎细胞因子产生的能力。它对脂肪组织中肿瘤坏死因子-α（TNF-α）和C反应蛋白（CRP）的表达具有负调控作用；降低血管和细胞内黏附分子（血管细胞黏附分子-1、细胞间黏附分子-1，即VCAM-1、ICAM-1）、E-选择素、白细胞介素-8（IL-8）的表达。高瘦素血症与高血压以及内皮功能障碍/动脉粥样硬化的发生有关，这是与心血管疾病发展相关的两个主要病理生理状况。瘦素介导的交感神经系统活动增加可能是引发肥胖相关高血压的主要机制之一。瘦素刺激促炎细胞因子的分泌，并增加内皮素-1（ET-1）的释放，这可能会促进高血压的发生。不对称二甲基精氨酸（ADMA）是一氧化氮（NO）生物合成的一种生理调节剂，血清水平升高会促进动脉粥样硬化进程，导致内皮功能障碍和心血管疾病的发生。
