Palomo Iván, Alarcón Marcelo, Moore-Carrasco Rodrigo, Argilés Josep M
Department of Clinical Biochemistry and Immunohematology, Faculty of Health Sciences, Universidad de Talca, Talca, Chile.
Int J Mol Med. 2006 Nov;18(5):969-74.
Metabolic syndrome (MS) is characterized by the presence of at least three of the following alterations: enlargement of the waist diameter, higher levels of arterial pressure, low density lipoprotein cholesterol and glycemia, and reduction of high density lipoprotein cholesterol. The prevalence of MS reaches 23% in young adults, a percentage that increases with age. People with MS have a greater risk of suffering from cardiovascular disease (CVD). The physiopathologic alterations now found to exist in MS are diverse; among them is endothelial dysfunction, which triggers atherogenic lesions and hypercoagulability characterized by alterations of the coagulation factors and the regulatory proteins of fibrinolysis such as the plasminogen activator inhibitor (PAI-1). The increase in oxidative stress and/or the reactive oxygen species in patients with MS is partially related to the oxidation state of the lipoproteins, especially of the low density lipoproteins. This fact favors atherogenesis. Moreover, the oxidative stress produces alterations in the production of adipokines, cytokines secreted by the adipose tissues. The abnormality in the transport of lipoprotein diminishes the catabolism of the very low density lipoprotein (VLDL) and increases the catabolism of the high density lipoprotein (HDL), which creates insulin resistance. This process is associated with a lower concentration of adiponectin that in turn regulates the catabolism of VLDL and HDL; consequently increasing the flow of fatty acids from the adipose tissue to the liver and muscles. The proinflammatory cytokines, among them tumor necrosis factor alpha (TNF-alpha), are of great importance in MS regulating different processes and molecules such as PAI-1. PAI-1 is controlled by the group of transcription factors peroxisome proliferator-activated receptor (PPAR), especially by PPAR gamma and alpha ligands. In summary, MS includes multiple alterations related to insulin resistance at several levels: hepatic, muscular, adipose and vascular tissue (endothelium). The exact mechanism that underlies the relationship between MS and CVD are not sufficiently known yet; pathogenic explanations are lacking for the mechanisms relating metabolic factors to insulin resistance and the association with the development of atherosclerosis and thrombosis. MS alterations and the main aspects related to homeostasis alterations are examined in this report.
代谢综合征（MS）的特征是存在以下至少三种改变：腰围增大、动脉压升高、低密度脂蛋白胆固醇和血糖水平升高，以及高密度脂蛋白胆固醇降低。MS在年轻人中的患病率达到23%，且该百分比随年龄增长而增加。患有MS的人患心血管疾病（CVD）的风险更高。目前发现MS中存在的生理病理改变多种多样；其中包括内皮功能障碍，它会引发动脉粥样硬化病变和高凝状态，其特征是凝血因子和纤维蛋白溶解调节蛋白（如纤溶酶原激活物抑制剂（PAI-1））的改变。MS患者氧化应激和/或活性氧物质的增加部分与脂蛋白的氧化状态有关，尤其是低密度脂蛋白。这一事实有利于动脉粥样硬化的发生。此外，氧化应激会导致脂肪组织分泌的细胞因子（脂联素）产生改变。脂蛋白转运异常会减少极低密度脂蛋白（VLDL）的分解代谢，增加高密度脂蛋白（HDL）的分解代谢，从而产生胰岛素抵抗。这一过程与脂联素浓度降低有关，脂联素进而调节VLDL和HDL的分解代谢；因此增加了脂肪酸从脂肪组织流向肝脏和肌肉的流量。促炎细胞因子，其中包括肿瘤坏死因子α（TNF-α），在MS中对调节不同过程和分子（如PAI-1）非常重要。PAI-1受过氧化物酶体增殖物激活受体（PPAR）转录因子组的控制，尤其是受PPARγ和α配体的控制。总之，MS在多个层面包括与胰岛素抵抗相关的多种改变：肝脏、肌肉、脂肪和血管组织（内皮）。MS与CVD之间关系的确切机制尚不完全清楚；对于代谢因素与胰岛素抵抗之间的机制以及与动脉粥样硬化和血栓形成发展的关联，缺乏致病解释。本报告探讨了MS的改变以及与体内稳态改变相关的主要方面。
