Insulin resistance and cardiovascular disease

Insulin resistance and cardiovascular disease
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DOI:
10.1016/s0895-7061(01)02078-7
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发表时间:
2001-06-01
影响因子:
3.2
通讯作者:
Goodfriend, TL
Goodfriend, TL
中科院分区:
医学3区
文献类型:
--
作者:
Egan, BM;Greene, EL;Goodfriend, TL

文献摘要

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心血管危险因素在肥胖个体中聚集。胰岛素抵抗作为一个共同的致病因素的风险因素集群。非酯化脂肪酸代谢的缺陷已牵连在异常的脂质和葡萄糖代谢的特点集群。其他证据也导致脂肪细胞作为危险因素簇和心血管并发症的重要贡献者,其不仅对脂肪酸,而且对瘦素、纤溶酶原激活物抑制剂-1和血管紧张素原的影响,仅举几例。脂肪酸在腹部肥胖个体中升高,对胰岛素抑制更有抵抗力,并可能导致高血压。脂肪酸可通过抑制内皮型一氧化氮合酶活性和损害内皮依赖性血管舒张作用来影响血压。脂肪酸增加α(1)-肾上腺素受体介导的血管反应性,并增强培养的血管平滑肌细胞的增殖和迁移。脂肪酸的几种作用是通过氧化应激介导的。脂肪酸还可以与簇的其他方面相互作用,包括增加血管紧张素II,以加重氧化应激。氧化应激反过来又与胰岛素抵抗、高血压、血管重塑和血管并发症的发病机制有关。更清楚地描述关键的活性氧信号通路以及各种干预措施对这些通路的影响,可以促进抗氧化治疗的合理方法,并改善快速增长的高风险、胰岛素抵抗、肥胖个体的结局。美国高血压杂志2001;14:116 S-125 S(C)2001年美国高血压杂志,有限公司。
Cardiovascular risk factors cluster in obese individuals. Insulin resistance emerges as a common pathogenetic denominator underlying the risk factor cluster. Defects in nonesterified fatty acids metabolism have been implicated in the abnormal lipid and glucose metabolism which characterize the cluster. Other evidence also leads to the adipocyte as an important contributor to the risk factor cluster and cardiovascular complications through effects not only on fatty acids but also on leptin, plasminogen activator inhibitor-1, and angiotensinogen, to name a few. Fatty acids are elevated among abdominally obese individuals, are more resistant to suppression by insulin, and may contribute to hypertension. Fatty acids may affect blood pressure by inhibiting endothelial nitric oxide synthase activity and impairing endothelium-dependent vasodilation. Fatty acids increase alpha (1)-adrenoceptor-mediated vascular reactivity and enhance the proliferation and migration of cultured vascular smooth-muscle cells. Several effects of fatty acids are mediated through oxidative stress. Fatty acids can also interact with other facets of cluster, including increased angiotensin II, to accentuate oxidative stress. Oxidative stress, in turn, is implicated in the pathogenesis of insulin resistance, hypertension, vascular remodeling, and vascular complications. A clearer delineation of the key reactive oxygen signaling pathways and the impact of various interventions on these pathways could facilitate a rationale approach to antioxidant therapy and improved outcomes among the rapidly growing number of high-risk, insulin-resistant, obese individuals. Am J Hypertens 2001;14:116S-125S (C) 2001 American Journal of Hypertension, Ltd.