Reaven G M
Department of Medicine, Stanford University School of Medicine, California 94305.
Annu Rev Med. 1993;44:121-31. doi: 10.1146/annurev.me.44.020193.001005.
Resistance to insulin-mediated glucose uptake is characteristic of individuals with impaired glucose intolerance or non-insulin-dependent diabetes, and it also occurs commonly in patients with high blood pressure. The physiological response to a decrease in insulin-mediated glucose uptake is an increase in insulin secretion, and as long as a state of compensatory hyperinsulinemia can be maintained, frank decompensation of glucose tolerance can be prevented. However, it is likely that the defect in insulin action and/or the associated hyperinsulinemia will lead to an increase in plasma triglyceride and a decrease in high density lipoprotein-cholesterol concentration, and high blood pressure. It seems likely that the cluster of changes associated with resistance to insulin-mediated glucose uptake comprise a syndrome, which plays an important role in the etiology and clinical course of patients with non-insulin-dependent diabetes, high blood pressure, and coronary heart disease.
胰岛素介导的葡萄糖摄取抵抗是糖耐量受损或非胰岛素依赖型糖尿病患者的特征，在高血压患者中也很常见。对胰岛素介导的葡萄糖摄取减少的生理反应是胰岛素分泌增加，只要能维持代偿性高胰岛素血症状态，就可以预防糖耐量的明显失代偿。然而，胰岛素作用缺陷和/或相关的高胰岛素血症可能会导致血浆甘油三酯升高、高密度脂蛋白胆固醇浓度降低以及高血压。与胰岛素介导的葡萄糖摄取抵抗相关的一系列变化似乎构成一种综合征，在非胰岛素依赖型糖尿病、高血压和冠心病患者的病因学和临床病程中起重要作用。
