Insulin Resistance, Hyperinsulinemia, Dyslipidemia, Hypertension, and Accelerated Atherosclerosis

Insulin Resistance, Hyperinsulinemia, Dyslipidemia, Hypertension, and Accelerated Atherosclerosis
复制标题

DOI:
10.1177/009127009203200607
复制
发表时间:
1992-06
期刊:
The Journal of Clinical Pharmacology
影响因子:
--
通讯作者:
J. Sowers
J. Sowers
中科院分区:
其他
文献类型:
--
作者:
J. Sowers

文献摘要

被引文献

相似文献

高血压只是多方面代谢-血流动力学复合体的一个组成部分,该复合体还包括肥胖、轻微和明显的糖耐量异常、血脂异常、血管阻力增强和加速的动脉粥样硬化。过去5年的许多研究结果表明,即使是非肥胖、非糖尿病的高血压患者也表现出胰岛素抵抗,这种抵抗位于外周组织(主要是骨骼肌),仅限于葡萄糖代谢的非氧化途径,而且似乎与高血压的严重程度直接相关。高血压患者的胰岛素抵抗和相关的高胰岛素血症也与血浆甘油三酯水平升高和高密度脂蛋白浓度降低有关,这可能是动脉粥样硬化加剧的原因之一。高胰岛素血症可能通过增加低密度脂蛋白在血管壁上的积聚、血管平滑肌的迁移和增殖、增加血管壁上结缔组织的合成和减少脂斑块的消退而直接促进动脉粥样硬化。外周血管阻力增强是胰岛素抵抗/高胰岛素血症状态的特征,可能与血管平滑肌对胰岛素的反应降低有关,胰岛素通常调节(减弱)血管收缩对血管活性物质的反应。
Hypertension is only one component of a multifaceted metabolic‐hemodynamic complex that also includes obesity, subtle and overt glucose intolerance, dyslipidemia, enhanced vascular resistance and accelerated atherosclerosis. Results of a number of studies in the past 5 years have shown that even nonobese, nondiabetic individuals with hypertension display insulin resistance, which is located in peripheral tissues (primarily skeletal muscle), is limited to nonoxidative pathways of glucose disposal, and appears to be directly correlated with the severity of hypertension. Insulin resistance and associated hyperinsulinemia in hypertensive individuals are also associated with increased plasma triglyceride levels and decreased high‐density lipoprotein concentrations, which likely contributes to enhanced atherosclerosis. Hyperinsuiinemia may directly promote atherosclerosis by enhancing LDL‐cholesterol accumulation in vessel walls, vascular smooth muscle migration, and proliferation, augmenting connective tissue synthesis in the vascular wall, and decreasing the regression of lipid plaques. The enhanced peripheral vascular resistance that characterizes insulin resistance/hyperinsu Jinemic states may be related to decreased vascular smooth muscle responses to insulin, which normally modulates (attenuates) vascular contractile responses to vasoactive agents.