Clark M G, Patten G S, Clark D G
Biochem J. 1984 Dec 15;224(3):863-9. doi: 10.1042/bj2240863.
The hormonal regulation of L-type pyruvate kinase in hepatocytes from phosphorylase b kinase-deficient (gsd/gsd) rats was investigated. Adrenaline (10 microM) and glucagon (10 nM) each led to an inactivation and phosphorylation of pyruvate kinase. Dose-response curves for adrenaline-mediated inactivation of pyruvate kinase, phosphorylation of pyruvate kinase and the stimulation of gluconeogenesis from 1.8 mM-lactate were similar for hepatocytes from control and gsd/gsd rats. Time-course studies indicated that adrenaline-mediated inactivation and phosphorylation of pyruvate kinase proceeded more slowly in phosphorylase kinase-deficient hepatocytes than in control hepatocytes. The age-dependent change in the adrenergic control of pyruvate kinase was similar between control and phosphorylase kinase-deficient hepatocytes. Adrenaline, glucagon and noradrenaline activated the cyclic AMP-dependent protein kinase and inhibited pyruvate kinase in phosphorylase kinase-deficient hepatocytes. Vasopressin (0.2-2 nM), angiotensin (10nM) and A23187 (10 microM) had no effect on the activity ratio of the cyclic AMP-dependent protein kinase or pyruvate kinase in these cells. It is concluded that phosphorylase kinase plays no significant role in the hormonal control of pyruvate kinase and that phosphorylation and inactivation of this enzyme results predominantly from the action of the cyclic AMP-dependent protein kinase.
对磷酸化酶b激酶缺陷型（gsd/gsd）大鼠肝细胞中L型丙酮酸激酶的激素调节进行了研究。肾上腺素（10微摩尔）和胰高血糖素（10纳摩尔）均可导致丙酮酸激酶失活和磷酸化。对于对照大鼠和gsd/gsd大鼠的肝细胞，肾上腺素介导的丙酮酸激酶失活、丙酮酸激酶磷酸化以及1.8毫摩尔乳酸糖异生刺激的剂量反应曲线相似。时间进程研究表明，在磷酸化酶激酶缺陷的肝细胞中，肾上腺素介导的丙酮酸激酶失活和磷酸化比对照肝细胞中进行得更慢。对照肝细胞和磷酸化酶激酶缺陷肝细胞中，丙酮酸激酶肾上腺素能控制的年龄依赖性变化相似。肾上腺素、胰高血糖素和去甲肾上腺素激活了环磷酸腺苷依赖性蛋白激酶，并在磷酸化酶激酶缺陷的肝细胞中抑制了丙酮酸激酶。血管加压素（0.2 - 2纳摩尔）、血管紧张素（10纳摩尔）和A23187（10微摩尔）对这些细胞中环磷酸腺苷依赖性蛋白激酶或丙酮酸激酶的活性比没有影响。得出的结论是，磷酸化酶激酶在丙酮酸激酶的激素控制中不起重要作用，并且该酶的磷酸化和失活主要是由环磷酸腺苷依赖性蛋白激酶的作用导致的。
