Lutaya G, Rodrigues L M, Griffiths J R
Biochem J. 1986 Oct 15;239(2):493-6. doi: 10.1042/bj2390493.
Sulphate ions have been known for some years to enhance the activity of hepatic glycogen phosphorylase b in vitro. Here we report that intravenous injections of 4.92 mmol of Na2SO4/kg body wt. to rats induced marked hepatic glycogenolysis in vivo, accompanied by polyuria, glycosuria and a mild hyperglycaemia. These effects were observed both in normal (Wistar) rats and in gsd/gsd rats that lacked hepatic phosphorylase kinase. In both rat strains the activity of glycogen phosphorylase in liver extracts was enhanced by pretreatment of the animals with Na2SO4, but in phosphorylase kinase-deficient livers the enhancement was solely in phosphorylase b activity, whereas both the a and b forms of the enzyme were activated in normal livers. Hepatic glycogenolysis was also induced by perfusing rat livers, both normal and gsd/gsd, with 25 mM-Na2SO4. Under these conditions both the rat strains showed only enhanced activities of glycogen phosphorylase b. This suggested that the increased activity of phosphorylase a in the extracts of normal livers after Na2SO4 administration in vivo was due to a hormonally mediated conversion of the b form into the a form. The activation of glycogen phosphorylase b was stable to dilution and appeared to be due to a long-lasting structural change in the enzyme or very tight binding of an activator.
多年来人们已知硫酸根离子在体外可增强肝糖原磷酸化酶b的活性。在此我们报告，给大鼠静脉注射4.92 mmol/kg体重的Na2SO4可在体内诱导明显的肝糖原分解，同时伴有多尿、糖尿和轻度高血糖。在正常（Wistar）大鼠和缺乏肝磷酸化酶激酶的gsd/gsd大鼠中均观察到了这些效应。在这两种大鼠品系中，用Na2SO4预处理动物可增强肝提取物中糖原磷酸化酶的活性，但在缺乏磷酸化酶激酶的肝脏中，增强的仅是磷酸化酶b的活性，而在正常肝脏中该酶的a型和b型均被激活。用25 mM - Na2SO4灌注正常和gsd/gsd大鼠的肝脏也可诱导肝糖原分解。在这些条件下，两种大鼠品系均仅表现出糖原磷酸化酶b的活性增强。这表明在体内给予Na2SO4后，正常肝脏提取物中磷酸化酶a活性的增加是由于激素介导的b型向a型的转化。糖原磷酸化酶b的激活对稀释稳定，似乎是由于该酶的持久结构变化或激活剂的紧密结合。
