Plas C, Menuelle P, Forest N, Pringault E
Reprod Nutr Dev (1980). 1983;23(2 B):421-8.
In the present study, we used primary cultures of fetal rat hepatocytes which are highly suitable for studying the glycogenic effect of insulin and its regulation. After a lag in the period of culture in the presence of cortisol, glycogenic response to insulin developed together with a progressive accumulation of glycogen. When insulin was added, the rate of glycogen synthesis increased, becoming maximal after 2-3 h, due to the activation of the glycogen synthase system already present. Modification of glycogen precursors in the medium did not alter the amplitude of the insulin effect. The glycogenic effect of insulin was unrelated to that of glucose load and occurred after the formation of glucose-1-phosphate. This only happened when the cyclic AMP-dependent glycogenolytic system was not stimulated, since it was suppressed by low doses of glucagon. Insulin effect, which was time-dependent, ceased after 4 h. This corresponded to a desensitization of hepatocytes without any alteration in the specific binding of insulin. These variations in the glycogenic effect of insulin were likely due to different causes; one of these could be the first events following the interaction of insulin with its receptor.
在本研究中，我们使用了原代培养的胎鼠肝细胞，这些细胞非常适合用于研究胰岛素的糖原生成作用及其调节机制。在存在皮质醇的培养期出现延迟后，对胰岛素的糖原生成反应随着糖原的逐渐积累而产生。添加胰岛素后，糖原合成速率增加，在2 - 3小时后达到最大值，这是由于已存在的糖原合酶系统被激活。培养基中糖原前体的改变并未改变胰岛素作用的幅度。胰岛素的糖原生成作用与葡萄糖负荷无关，且在葡萄糖 - 1 - 磷酸形成后发生。这仅在环磷酸腺苷依赖性糖原分解系统未被刺激时发生，因为低剂量的胰高血糖素可抑制该系统。胰岛素的作用具有时间依赖性，4小时后停止。这对应于肝细胞的脱敏，而胰岛素的特异性结合没有任何改变。胰岛素糖原生成作用的这些变化可能是由不同原因引起的；其中之一可能是胰岛素与其受体相互作用后的初始事件。
