Quentmeier A, Klein H, Unthan-Fechner K, Probst I
Institut für Biochemie, Fachbereich Medizin, Georg-August-Universität Göttingen.
Biol Chem Hoppe Seyler. 1993 Oct;374(10):965-71. doi: 10.1515/bchm3.1993.374.7-12.965.
Phenylarsine oxide (PAO), a trivalent arsenical which complexes vicinal dithiols, prevented the action of insulin in primary cultured adult rat hepatocytes. Simultaneous short-term treatment of 48-h old cells with insulin and 2 microM PAO resulted in complete attenuation of the insulin-dependent increase in the level of fructose 2,6-bisphosphate and the activation of phosphofructokinase 2, pyruvate kinase, glucokinase flux and glycolysis. Basal rates of glucose transport and glycolysis were not affected. PAO also abolished stimulation of glycogen synthesis and amino-acid transport and the decrease of glycogenolysis evoked by insulin. The 20-fold activation of the insulin receptor tyrosine kinase by insulin was, however, not reduced by PAO. The data suggest that in differentiated hepatocytes insulin signal transduction involves vicinal sulhydryls located at a post-receptor step.
苯胂化氧（PAO）是一种能与邻二硫醇络合的三价砷化合物，它可抑制原代培养的成年大鼠肝细胞中胰岛素的作用。对48小时龄的细胞同时进行短期胰岛素和2微摩尔PAO处理，会使果糖2,6 - 二磷酸水平的胰岛素依赖性增加以及磷酸果糖激酶2、丙酮酸激酶、葡萄糖激酶通量和糖酵解的激活完全减弱。葡萄糖转运和糖酵解的基础速率不受影响。PAO还消除了胰岛素对糖原合成和氨基酸转运的刺激以及对糖原分解的抑制作用。然而，PAO并未降低胰岛素对胰岛素受体酪氨酸激酶的20倍激活作用。这些数据表明，在分化的肝细胞中，胰岛素信号转导涉及位于受体后步骤的邻巯基。
