Becker S G, Smollin P F, Richardson D K, Czech M P
Horm Metab Res. 1978 May;10(3):204-8. doi: 10.1055/s-0028-1093435.
In the presence of 5mM glucose insulin only modestly activated rates of glucose uptake by rat epitrochlearis muscles while the rate of glycogen formation from D(U-14C) glucose was markedly stimulated by the hormone. No effect of insulin on lactate output could be detected under these conditions. The activation of labeled glycogen formation by insulin occurred in a dose-dependent manner and a maximal effect was noted at hormone concentrations greater than 4 mU/ml. However, glycogen accumulation by epitrochlearis muscles obtained from old, spontaneously obese rats was activated by only 38 +/- 15% by a supermaximal insulin concentration (200 mU/ml) compared to a 123 +/- 43% stimulation observed in muscles from small rats. This impaired responsiveness to the hormone could not be explained by inhibition of the glycogen synthetase system by increased amounts of endogenous glycogen in the epitrochlearis muscle of spontaneously obese rats. The magnitude of this resistance greatly exceeds the modest reduction in insulin receptor number reported for msucle membranes in obese rats which suggests that other defective cellular components contribute to this syndrome.
在5mM葡萄糖存在的情况下，胰岛素仅适度激活大鼠肱三头肌的葡萄糖摄取速率，而D（U-14C）葡萄糖的糖原形成速率则受到该激素的显著刺激。在这些条件下，未检测到胰岛素对乳酸输出的影响。胰岛素对标记糖原形成的激活呈剂量依赖性，在激素浓度大于4 mU/ml时观察到最大效应。然而，与在幼鼠肌肉中观察到的123±43%的刺激相比，来自老年自发性肥胖大鼠的肱三头肌通过超最大胰岛素浓度（200 mU/ml）仅激活了38±15%的糖原积累。这种对激素反应性受损不能用自发性肥胖大鼠肱三头肌中内源性糖原量增加对糖原合成酶系统的抑制来解释。这种抵抗的程度大大超过了肥胖大鼠肌肉膜中报道的胰岛素受体数量的适度减少，这表明其他有缺陷的细胞成分导致了这种综合征。
