Bełtowski Jerzy, Jamroz-Wiśniewska Anna, Widomska Sylwia
Department of Pathophysiology, Medical University, Lublin, Poland.
Cardiovasc Hematol Disord Drug Targets. 2008 Mar;8(1):7-46. doi: 10.2174/187152908783884920.
Studies performed during the last decade indicate that adipose tissue is not only a site of triglyceride storage but also an active endocrine organ which secretes many biologically active mediators referred to as "adipokines". In contrast to many adipokines which are overproduced in obese individuals and exert deleterious effects on insulin sensitivity, lipoprotein metabolism and cardiovascular system, such as leptin, tumor necrosis factor-alpha, plasminogen activator inhibitor-1, resistin, etc., adiponectin seems to be a unique adipokine which is produced in lower amounts in obese than in lean subjects and possesses predominantly beneficial activities, i.e. increases insulin sensitivity, stimulates fatty acid oxidation, inhibits inflammatory reaction and induces endothelium-dependent nitric oxide-mediated vasorelaxation. Adiponectin binds two receptors, AdipoR1 and AdipoR2. Adiponectin knockout mice exhibit various manifestations of the metabolic syndrome such as insulin resistance, glucose intolerance, hyperlipidemia, impaired endothelium-dependent vasorelaxation and hypertension, as well as augmented neointima formation after vascular injury. Clinical studies indicate that plasma adiponectin concentration is lower in patients with essential hypertension and ischemic heart disease. Raising endogenous adiponectin level or increasing the sensitivity to this hormone may be a promising therapeutic strategy for patients with metabolic and cardiovascular diseases. Among currently used drugs, thiazolidinediones (peroxisome proliferator activated receptor gamma agonists) are most effective in elevating adiponectin level.
过去十年进行的研究表明，脂肪组织不仅是甘油三酯储存的场所，还是一个活跃的内分泌器官，它分泌许多被称为“脂肪因子”的生物活性介质。与许多在肥胖个体中过度产生并对胰岛素敏感性、脂蛋白代谢和心血管系统产生有害影响的脂肪因子不同，如瘦素、肿瘤坏死因子-α、纤溶酶原激活物抑制剂-1、抵抗素等，脂联素似乎是一种独特的脂肪因子，在肥胖者中产生的量低于瘦人，且主要具有有益活性，即提高胰岛素敏感性、刺激脂肪酸氧化、抑制炎症反应并诱导内皮依赖性一氧化氮介导的血管舒张。脂联素与两种受体AdipoR1和AdipoR2结合。脂联素基因敲除小鼠表现出代谢综合征的各种表现，如胰岛素抵抗、葡萄糖不耐受、高脂血症、内皮依赖性血管舒张受损和高血压，以及血管损伤后新内膜形成增加。临床研究表明，原发性高血压和缺血性心脏病患者的血浆脂联素浓度较低。提高内源性脂联素水平或增加对该激素的敏感性可能是治疗代谢和心血管疾病患者的一种有前景的治疗策略。在目前使用的药物中，噻唑烷二酮类（过氧化物酶体增殖物激活受体γ激动剂）在提高脂联素水平方面最有效。
