Grundy Scott M
Center for Human Nutrition University of Texas Southwestern Medical Center Dallas, Texas 75390-9052, USA.
Clin Cornerstone. 2006;8 Suppl 1:S21-7. doi: 10.1016/s1098-3597(06)80005-0.
Atherogenic dyslipidemia, a component of metabolic syndrome, is characterized by high levels of apolipoprotein B (apo B)-containing lipoproteins, including very-low-density lipoprotein remnants and small low-density lipoprotein particles, and reduced levels of high-density lipoprotein cholesterol. Although the National Cholesterol Education Program Adult Treatment Panel III includes elevations in blood pressure and plasma glucose in the definition of metabolic syndrome, the broader scope of metabolic syndrome includes proinflammatory and prothrombotic states, which derive from the secretory activity of adipose tissue. Abdominal fat can adversely affect insulin action and the disposal of glucose through an increase in the release of free fatty acid, resulting in accumulation of triglyceride in muscle and liver, thereby depressing insulin action and increasing output of apo B-containing lipoproteins. Impaired regulation of adipokines, bioactive substances secreted from adipose tissue, likely produces systemic inflammation, which can promote atherogenesis. Insulin resistance is recognized as an important metabolic defect linking the components of metabolic syndrome. One molecule that may play an important role in metabolic syndrome to regulate metabolic and vascular pathways is the peroxisome proliferator-activated receptor-gamma (PPAR-gamma). Studies have established PPAR-gamma deficiency as a cause of lipodystrophy and confirmed its adipogenic role. Patients with atherogenic dyslipidemia and metabolic syndrome should undergo global risk assessment for cardiovascular disease and future cardiovascular events to determine an overall treatment strategy.
致动脉粥样硬化性血脂异常是代谢综合征的一个组成部分，其特征是含有载脂蛋白B（apo B）的脂蛋白水平升高，包括极低密度脂蛋白残粒和小的低密度脂蛋白颗粒，以及高密度脂蛋白胆固醇水平降低。尽管美国国家胆固醇教育计划成人治疗专家组第三次报告在代谢综合征的定义中纳入了血压和血糖升高，但代谢综合征更广泛的范畴包括源自脂肪组织分泌活动的促炎和促血栓形成状态。腹部脂肪可通过增加游离脂肪酸的释放对胰岛素作用和葡萄糖代谢产生不利影响，导致甘油三酯在肌肉和肝脏中蓄积，从而抑制胰岛素作用并增加含apo B脂蛋白的输出。脂肪组织分泌的生物活性物质——脂肪因子的调节受损，可能会引发全身炎症，进而促进动脉粥样硬化的发生。胰岛素抵抗被认为是连接代谢综合征各组成部分的一个重要代谢缺陷。过氧化物酶体增殖物激活受体γ（PPAR-γ）可能是在代谢综合征中调节代谢和血管通路发挥重要作用的一个分子。研究已证实PPAR-γ缺乏是脂肪营养不良的一个病因，并确认了其在脂肪生成中的作用。患有致动脉粥样硬化性血脂异常和代谢综合征的患者应接受心血管疾病及未来心血管事件的全面风险评估，以确定总体治疗策略。
