Reaven G M
Adv Exp Med Biol. 1985;189:129-36. doi: 10.1007/978-1-4757-1850-8_8.
In conclusion, there is considerable data documenting the presence of resistance to insulin-stimulated glucose uptake in patients with either IDDM or NIDDM. However, the characteristics of this metabolic abnormality are quite different in the two syndromes. In the case of IDDM the insulin resistance appears to be secondary to the state of altered carbohydrate homeostasis, is directly proportional to the severity of fasting hyperglycemia, and can be abolished by achievement of metabolic control. As a corollary, it seems reasonable to suggest that resistance to insulin-stimulated glucose uptake is not a primary defect in the pathogenesis of IDDM. Nevertheless, the presence of insulin resistance in the poorly-controlled patient with IDDM may be of great clinical relevance, and contribute to the difficulty in effective treatment of this syndrome. In contrast, resistance to insulin-stimulated glucose uptake does not seem to be a simple function of severity of hyperglycemia in patients with NIDDM, and significant insulin resistance can exist in these patients in association with only mild carbohydrate intolerance. Furthermore, although the decline in insulin-stimulated glucose disposal present in patients with significant fasting hyperglycemia can be increased by instituting excellent metabolic control with exogenous insulin, it cannot be restored to normal. These observations suggest that some component of the insulin resistance in NIDDM is similar to that in IDDM, and is secondary to the state of poor metabolic control. On the other hand, it also suggests that another component of the insulin resistance in NIDDM is primary, and most likely related to the pathogenesis of this syndrome. Obviously, there is a great need to define the mechanism of this unexplained portion of the insulin resistance of NIDDM.
总之，有大量数据证明胰岛素依赖型糖尿病（IDDM）或非胰岛素依赖型糖尿病（NIDDM）患者存在对胰岛素刺激的葡萄糖摄取的抵抗。然而，这种代谢异常在这两种综合征中的特征有很大不同。在IDDM患者中，胰岛素抵抗似乎继发于碳水化合物稳态改变的状态，与空腹高血糖的严重程度成正比，并且可以通过实现代谢控制而消除。由此推论，提示对胰岛素刺激的葡萄糖摄取的抵抗不是IDDM发病机制中的原发性缺陷似乎是合理的。尽管如此，IDDM控制不佳的患者中胰岛素抵抗的存在可能具有重要的临床意义，并导致该综合征有效治疗的困难。相比之下，NIDDM患者对胰岛素刺激的葡萄糖摄取的抵抗似乎并非高血糖严重程度的简单函数，并且这些患者中仅伴有轻度碳水化合物不耐受时也可能存在显著的胰岛素抵抗。此外，虽然通过外源性胰岛素实现良好的代谢控制可增加空腹高血糖显著的患者中胰岛素刺激的葡萄糖清除率的下降，但无法恢复至正常。这些观察结果提示，NIDDM中胰岛素抵抗的某些成分与IDDM中的相似，并且继发于代谢控制不佳的状态。另一方面，这也提示NIDDM中胰岛素抵抗的另一个成分是原发性的，并且很可能与该综合征的发病机制有关。显然，非常有必要明确NIDDM中这种无法解释的胰岛素抵抗部分的机制。
