Nemenoff R A, Blackshear P J, Avruch J
J Biol Chem. 1983 Aug 10;258(15):9437-43.
An inhibitor (inhibitor-1) of phosphorylase a phosphatase has been identified in rat epididymal fat pads. This heat-stable, acid-soluble protein only exhibits phosphatase inhibitory activity when it itself is phosphorylated. Inhibitor-1 in rat adipose tissue migrates at 32,000 Da on sodium dodecyl sulfate-polyacrylamide gels, and at 64,000 Da on gel filtration. Exposure of fat pads to insulin (1 milliunit/ml) resulted in a 50% decrease in inhibitor-1 activity, compared to control (p less than 0.001). Isoproterenol (10(-6) M) caused a 25% increase in inhibitor-1 activity (p less than 0.05). Electrophoresis of heat-stable proteins prepared from hormone-treated 32P-labeled fat cells showed that insulin caused a dephosphorylation of the 32,000 Da phosphoprotein by 30% (p less than 0.01), whereas isoproterenol stimulated 32P incorporation in this protein by 35% compared to control (p less than 0.05). Thus, insulin appears to dephosphorylate and inactivate inhibitor-1, and might thereby result in an increase of protein phosphatase activity. Insulin regulation of inhibitor-1 is a mechanism which may underlie other of insulin's effects in adipose tissue, such as the activation of glycogen synthase.
在大鼠附睾脂肪垫中已鉴定出一种磷酸化酶a磷酸酶的抑制剂(抑制剂-1)。这种热稳定的酸性可溶性蛋白只有在自身磷酸化时才表现出磷酸酶抑制活性。大鼠脂肪组织中的抑制剂-1在十二烷基硫酸钠-聚丙烯酰胺凝胶上的迁移分子量为32,000 Da,在凝胶过滤中的迁移分子量为64,000 Da。与对照组相比,将脂肪垫暴露于胰岛素(1毫单位/毫升)会导致抑制剂-1活性降低50%(p<0.001)。异丙肾上腺素(10^(-6) M)使抑制剂-1活性增加25%(p<0.05)。对经激素处理的32P标记脂肪细胞制备的热稳定蛋白进行电泳显示,胰岛素使32,000 Da磷蛋白的去磷酸化程度达30%(p<0.01),而异丙肾上腺素与对照组相比使该蛋白中的32P掺入量增加35%(p<0.05)。因此,胰岛素似乎使抑制剂-1去磷酸化并使其失活,从而可能导致蛋白磷酸酶活性增加。胰岛素对抑制剂-1的调节是一种机制,可能是胰岛素在脂肪组织中其他作用(如糖原合酶激活)的基础。