Pacholczyk Marta, Ferenc Tomasz, Kowalski Jan
Zakład Biologii i Genetyki Uniwersytetu Medycznego w Łodzi, Łódź.
Postepy Hig Med Dosw (Online). 2008 Oct 16;62:543-58.
The metabolic syndrome is a cluster of interrelated metabolic factors such as insulin resistance, hyperinsulinemia, abdominal obesity, impaired glucose tolerance, dyslipidemia, hypertension, and a proinflammatory and prothrombotic state. It is a common cause of the development of atherosclerotic vascular disease and type 2 diabetes. Genetic predisposition and environmental factors such as physical inactivity and increased caloric intake are responsible for the predisposition to metabolic syndrome. Available studies on the pathogenesis of metabolic syndrome are discrepant. Insulin resistance and abdominal obesity are the dominant causes of metabolic syndrome. Increased visceral adipose tissue mass and its proinflammatory activity are thought to underlie all the changes observed in metabolic syndrome. Adipose tissue is a dynamic endocrine and paracrine organ that produces and secretes inflammatory factors called adipokines, which link obesity, insulin resistance, atherosclerosis, and type 2 diabetes. Recent data suggest that oxidative stress is a primary pathogenic mechanism leading to the development of insulin resistance associated with over-nutrition. In this study the authors analyze the association between abdominal obesity, hyperinsulinemia, and insulin resistance and show some pathogenic mechanisms which may be responsible for the proatherogenic action of insulin resistance, hyperinsulinemia, and impaired glucose tolerance. Here the association among the disorders mentioned in the definitions of metabolic syndrome is discussed in more detail and it is shown that their clustering is not accidental in patients with insulin resistance. The role of adipose tissue in the development of insulin resistance and metabolic syndrome leading to overt cardiovascular disease and type 2 diabetes is also described.
代谢综合征是一组相互关联的代谢因素，如胰岛素抵抗、高胰岛素血症、腹型肥胖、糖耐量受损、血脂异常、高血压以及促炎和促血栓形成状态。它是动脉粥样硬化性血管疾病和2型糖尿病发生发展的常见原因。遗传易感性以及诸如缺乏身体活动和热量摄入增加等环境因素是导致代谢综合征易感性的原因。关于代谢综合征发病机制的现有研究存在差异。胰岛素抵抗和腹型肥胖是代谢综合征的主要原因。内脏脂肪组织量增加及其促炎活性被认为是代谢综合征中观察到的所有变化的基础。脂肪组织是一个动态的内分泌和旁分泌器官，它产生并分泌称为脂肪因子的炎症因子，这些因子将肥胖、胰岛素抵抗、动脉粥样硬化和2型糖尿病联系起来。最近的数据表明，氧化应激是导致与营养过剩相关的胰岛素抵抗发展的主要致病机制。在本研究中，作者分析了腹型肥胖、高胰岛素血症和胰岛素抵抗之间的关联，并展示了一些可能导致胰岛素抵抗、高胰岛素血症和糖耐量受损的促动脉粥样硬化作用的致病机制。在此更详细地讨论了代谢综合征定义中提及的疾病之间的关联，并表明它们在胰岛素抵抗患者中的聚集并非偶然。还描述了脂肪组织在导致明显心血管疾病和2型糖尿病的胰岛素抵抗和代谢综合征发展中的作用。
