Center for Human Nutrition, Washington University School of Medicine, 660 South Euclid Avenue, St Louis, MO 63110-1093, USA.
J Clin Hypertens (Greenwich). 2009 Dec;11(12):761-5. doi: 10.1111/j.1559-4572.2009.00054.x.
The cardiometabolic syndrome represents a cluster of metabolic abnormalities that are risk factors for cardiovascular disease. The mechanism(s) responsible for developing the cardiometabolic syndrome is not known, but it is likely that multi-organ insulin resistance, which is a common feature of the cardiometabolic syndrome, is involved. Insulin resistance is an important risk factor for type 2 diabetes and can cause vasoconstriction and renal sodium reabsorption, leading to increased blood pressure. Alterations in adipose tissue fatty acid and adipokine metabolism are involved in the pathogenesis of insulin resistance. Excessive rates of fatty acid release into the bloodstream can impair the ability of insulin to stimulate muscle glucose uptake and suppress hepatic glucose production. Noninfectious systemic inflammation associated with adipocyte and adipose tissue macrophage cytokine production can also cause insulin resistance. In addition, increased free fatty acid delivery to the liver can stimulate hepatic very low-density lipoprotein triglyceride production, leading to dyslipidemia.
代谢综合征是一组代谢异常的病症，是心血管疾病的危险因素。导致代谢综合征的机制尚不清楚，但很可能涉及多器官胰岛素抵抗，这是代谢综合征的一个共同特征。胰岛素抵抗是 2 型糖尿病的一个重要危险因素，可引起血管收缩和肾脏钠重吸收，导致血压升高。脂肪组织脂肪酸和脂肪因子代谢的改变参与了胰岛素抵抗的发病机制。过多的脂肪酸释放到血液中会损害胰岛素刺激肌肉摄取葡萄糖和抑制肝脏葡萄糖产生的能力。与脂肪细胞和脂肪组织巨噬细胞细胞因子产生相关的非传染性全身炎症也会导致胰岛素抵抗。此外，向肝脏输送更多的游离脂肪酸会刺激肝脏极低密度脂蛋白甘油三酯的产生，导致血脂异常。
