Waldhäusl W, Bratusch-Marrain P
Wien Klin Wochenschr. 1985 Apr 12;97(8):359-63.
Insulin resistance is a well-known phenomenon in diabetic patients. Its occurrence in Type 1 (insulin-dependent) diabetes is thought to be due both to metabolic and immunological disturbances. In this context, a key role is attributed to the augmented release of the 'diabetogenic' hormones, adrenaline, glucagon, cortisol and growth hormone, as well as to hypertonic dehydration and to the presence of insulin-binding antibodies. In this connection it is noteworthy that among the 'diabetogenic' hormones adrenaline exerts the strongest insulin-antagonistic effect and that hypertonic dehydration is associated with impairment of insulin action and of non-insulin-dependent hepatic glucose uptake (in vitro), while hypotonic rehydration reduces the elevated hepatic glucose production in dehydrated Type 1 diabetic patients. By contrast, the generally only slightly elevated serum insulin-binding capacity in insulin-treated diabetics is probably of least importance in the development of insulin resistance, unless excessively high insulin antibody titres prevail.
胰岛素抵抗在糖尿病患者中是一种众所周知的现象。1型(胰岛素依赖型)糖尿病患者出现胰岛素抵抗被认为是代谢和免疫紊乱共同作用的结果。在这种情况下,“致糖尿病”激素(肾上腺素、胰高血糖素、皮质醇和生长激素)的释放增加、高渗性脱水以及胰岛素结合抗体的存在被认为起着关键作用。值得注意的是,在“致糖尿病”激素中,肾上腺素具有最强的胰岛素拮抗作用,高渗性脱水与胰岛素作用受损以及非胰岛素依赖的肝脏葡萄糖摄取受损(体外实验)相关,而低渗性补液可降低1型糖尿病脱水患者升高的肝脏葡萄糖生成。相比之下,胰岛素治疗的糖尿病患者中血清胰岛素结合能力通常仅略有升高,这在胰岛素抵抗的发生中可能是最不重要的因素,除非存在过高的胰岛素抗体滴度。