Storey K B
J Biol Chem. 1987 Feb 5;262(4):1670-3.
Kinetic properties of regulatory enzymes of glycolysis in liver of the mouse, Zapus hudsonius, were modified during hibernation, the probable mechanism being covalent modification. Liver glycogen phosphorylase activity was strongly depressed during both short (less than 24 h) and long (5-8 days) term hibernation, the mechanism involving a decrease in both the percentage of enzyme in the active a form and the total amount (a + b) of enzyme expressed. Phosphofructokinase showed kinetic changes (a 2.5-fold increase in Ka for fructose-2,6-P2, 4- and 3.7-fold decreases in I50 values for ATP and citrate, compared to euthermic controls) in liver of hibernators indicative of phosphorylation inactivation of the enzyme. Measured levels of fructose-2,6-P2 in liver did not change during hibernation. Changes in pyruvate kinase kinetics in liver from long term hibernators similarly indicated enzyme phosphorylation in the depressed state (Ka for fructose-1,6-P2 increased 4.4-fold, I50 for L-alanine decreased 6.3-fold). Apparent covalent modification of glycolytic enzymes during hibernation may serve two functions: depression of glycolytic activity as part of the general metabolic rate depression of hibernation, or reorganization of fuel use in the hibernating state to limit carbohydrate catabolism and promote gluconeogenesis.
在冬眠期间，小鼠（美洲林跳鼠）肝脏中糖酵解调节酶的动力学特性发生了改变，可能的机制是共价修饰。在短期（少于24小时）和长期（5 - 8天）冬眠期间，肝脏糖原磷酸化酶的活性均显著降低，其机制包括活性a型酶的百分比以及所表达的酶总量（a + b）均下降。磷酸果糖激酶在冬眠动物的肝脏中显示出动力学变化（与正常体温对照相比，果糖-2,6-二磷酸的Ka增加2.5倍，ATP和柠檬酸的I50值分别降低4倍和3.7倍），表明该酶发生了磷酸化失活。在冬眠期间，肝脏中果糖-2,6-二磷酸的测量水平没有变化。长期冬眠动物肝脏中丙酮酸激酶动力学的变化同样表明该酶在抑制状态下发生了磷酸化（果糖-1,6-二磷酸的Ka增加4.4倍，L-丙氨酸的I50降低6.3倍）。冬眠期间糖酵解酶明显的共价修饰可能有两个作用：作为冬眠时总体代谢率降低的一部分，降低糖酵解活性；或者在冬眠状态下重新组织燃料利用，以限制碳水化合物分解代谢并促进糖异生。
