Hopkirk T J, Bloxham D P
Biochem J. 1979 Aug 15;182(2):383-97. doi: 10.1042/bj1820383.
Metabolic and enzymic changes were measured in meal-trained rats fed on high-carbohydrate diet. Rates of hepatic fatty acid synthesis are probably greater than rates of gluconeogenesis throughout the 24 h day provided that animals are fed. The daily enhancement of fatty acid synthesis on meal feeding coincided with the maximum activation of hepatic pyruvate kinase. Maximum activation of this enzyme was reflected in increased total catalytic activity (Vmax.), increased activity at 0.5 MM-phosphoenolpyruvate (V0.5), decreased Vmax./V0.5 ratio and a decrease in co-operativity of phosphoenolpyruvate binding as measured by the Hill coefficient (h). The latter changes are consistent with a decrease in enzyme phosphorylation during activation of the enzyme. To estimate changes in enzyme protein, quantitative enzyme precipitation with rabbit antisera was used. Giving a high-carbohydrate diet to meal-trained animals induced enzyme synthesis within a few hours. Adaptations in diet that enhanced fatty acid synthesis (chow to high carbohydrate; starved to high carbohydrate) led to an increased steady-state concentration of pyruvate kinase protein. An approximate estimate of the half-life of hepatic pyruvate kinase was 56 h. Whenever pyruvate kinase specific activity was measured in liver tissue extracts it was always considerably less (20--100 mumol/min per mg of protein, depending on dietary status) than the specific activity of pure pyruvate kinase (200 mumol/min per mg of protein). Antigenically active, catalytically inactive protein was removed during enzyme purification from cytosol at the stage of (NH4)2SO4 fractionation. The fraction precipitated by 30--45%-satd. (NH4)2SO4 was enzymically active, antigenically reacting protein was identified in the remaining (NH4)2SO4 fractions (0--30%- and 45--85%-satd.) and this contained no enzyme activity. These may correspond to inactive proteolytic fragments of pyruvate kinase. The rate-determining step in adjusting enzyme concentration seems to be proteolysis.
对以高碳水化合物饮食喂养的定时进餐训练大鼠的代谢和酶变化进行了测量。只要动物进食,在全天24小时内,肝脏脂肪酸合成速率可能大于糖异生速率。定时进餐时脂肪酸合成的每日增强与肝脏丙酮酸激酶的最大激活相吻合。该酶的最大激活表现为总催化活性(Vmax)增加、在0.5 mM磷酸烯醇丙酮酸时的活性(V0.5)增加、Vmax/V0.5比值降低以及通过希尔系数(h)测量的磷酸烯醇丙酮酸结合协同性降低。后一种变化与酶激活过程中酶磷酸化的减少一致。为了估计酶蛋白的变化,使用兔抗血清进行定量酶沉淀。给定时进餐训练的动物喂食高碳水化合物饮食会在数小时内诱导酶合成。饮食的调整增强了脂肪酸合成(普通饲料改为高碳水化合物;饥饿改为高碳水化合物),导致丙酮酸激酶蛋白的稳态浓度增加。肝脏丙酮酸激酶的半衰期约为56小时。每当在肝组织提取物中测量丙酮酸激酶比活性时,其总是比纯丙酮酸激酶的比活性(每毫克蛋白质200 μmol/min)低得多(20 - 100 μmol/min每毫克蛋白质,取决于饮食状态)。在从细胞溶胶中进行酶纯化的硫酸铵分级分离阶段,抗原活性但催化无活性的蛋白被去除。由30 - 45%饱和度硫酸铵沉淀的部分具有酶活性,在其余硫酸铵部分(0 - 30%饱和度和45 -
85%饱和度)中鉴定出抗原反应性蛋白,且该部分无酶活性。这些可能对应于丙酮酸激酶的无活性蛋白水解片段。调节酶浓度的限速步骤似乎是蛋白水解。