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非胰岛素依赖型(II型)糖尿病中胰岛素抵抗的机制。

Mechanisms of insulin resistance in non-insulin-dependent (type II) diabetes.

作者信息

Olefsky J M, Ciaraldi T P, Kolterman O G

出版信息

Am J Med. 1985 Sep 20;79(3B):12-22. doi: 10.1016/s0002-9343(85)80003-6.

Abstract

Characteristic of both obesity and non-insulin-dependent diabetes mellitus, insulin resistance is triggered at the level of the target tissue and can be induced by three general categories of causes: (1) an abnormal beta cell secretory product, (2) circulating insulin antagonists, or (3) a target tissue defect in insulin action. Decreased numbers of insulin receptors and a post-receptor defect in insulin action both play relative roles in insulin resistance. A general trend, however, indicates that as insulin resistance increases, the post-receptor defect becomes more prominent. Impaired glucose uptake and subsequent increased hepatic glucose oxidation in non-insulin-dependent diabetes mellitus are major contributing factors to fasting hyperglycemia.

摘要

胰岛素抵抗是肥胖症和非胰岛素依赖型糖尿病的共同特征,它在靶组织水平被触发,可由三大类原因引起:(1)异常的β细胞分泌产物,(2)循环胰岛素拮抗剂,或(3)胰岛素作用的靶组织缺陷。胰岛素受体数量减少以及胰岛素作用的受体后缺陷在胰岛素抵抗中均起相关作用。然而,总体趋势表明,随着胰岛素抵抗增加,受体后缺陷变得更加突出。非胰岛素依赖型糖尿病中葡萄糖摄取受损以及随后肝脏葡萄糖氧化增加是空腹高血糖的主要促成因素。

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