Tóth B, Bollen M, Stalmans W
Afdeling Biochemie, Faculteit Geneeskunde, Katholieke Universiteit Leuven, Belgium.
J Biol Chem. 1988 Oct 5;263(28):14061-6.
The intravenous administration of glucagon to anesthetized rats resulted within 5 min in a 20% drop in the hepatic phosphorylase phosphatase activity, as measured in a post-mitochondrial supernatant at low dilution, but it did not affect the activity of glycogensynthase phosphatase. On the other hand, the injection of insulin plus glucose caused increases by about 35% in both phosphatase activities. Upon subcellular fractionation these effects were recovered in the cytosol, but not in the glycogen/microsomal fraction. However, activity changes in the latter fraction were observed after recombination with the liver cytosol from a hormone-treated animal. Preincubation of the liver cytosol with modulator protein (a specific inhibitor of type-1 protein phosphatases) cancelled the activity changes induced by insulin plus glucose. No hormonal effects on hepatic protein phosphatase activities were observed when the fractions were either diluted an additional 10-fold or pretreated with trypsin. An acute hormonal regulation of protein phosphatases could also be demonstrated in the perfused liver. When added to the perfusion medium, glucose as well as insulin increased the cytosolic protein phosphatase activities by about 25%. Their effect was additive, irrespective of the order of addition. On the other hand, the addition of glucagon and/or vasopressin resulted in a 20% drop in the phosphorylase phosphatase activity. The presence of glucagon did not interfere with the effectiveness of insulin, and vice versa. The changes in the phosphorylase phosphatase activities induced by glucagon, insulin, and glucose represented changes in the Vmax only. We propose that the acute control of the hepatic glycogen synthase phosphatase and phosphorylase phosphatase activities is mediated by transferable, cytosolic effector(s).
给麻醉大鼠静脉注射胰高血糖素后5分钟内,低稀释度线粒体后上清液中测得的肝磷酸化酶磷酸酶活性下降了20%,但不影响糖原合酶磷酸酶的活性。另一方面,注射胰岛素加葡萄糖使两种磷酸酶活性均增加约35%。经亚细胞分级分离后,这些效应在胞质溶胶中得以恢复,但在糖原/微粒体部分未恢复。然而,与激素处理动物的肝细胞溶胶重组后,观察到后一部分的活性发生了变化。肝细胞溶胶与调节蛋白(1型蛋白磷酸酶的特异性抑制剂)预孵育可消除胰岛素加葡萄糖诱导的活性变化。当各部分再稀释10倍或用胰蛋白酶预处理时,未观察到激素对肝蛋白磷酸酶活性的影响。在灌注肝脏中也可证明蛋白磷酸酶的急性激素调节作用。当加入灌注培养基中时,葡萄糖以及胰岛素可使胞质蛋白磷酸酶活性增加约25%。它们的作用是相加的,与添加顺序无关。另一方面,加入胰高血糖素和/或血管加压素会导致磷酸化酶磷酸酶活性下降20%。胰高血糖素的存在不干扰胰岛素的作用,反之亦然。胰高血糖素、胰岛素和葡萄糖诱导的磷酸化酶磷酸酶活性变化仅代表Vmax的变化。我们认为,肝糖原合酶磷酸酶和磷酸化酶磷酸酶活性的急性控制是由可转移的胞质效应物介导的。