Zemplényl T, Rosenstein A J
Atherosclerosis. 1975 Mar-Apr;21(2):167-77. doi: 10.1016/0021-9150(75)90078-7.
The activity of phosphofructokinase (PFK, 2.7.1.11) was measured in arteries of very young (5-8 week old) pigeons known to differ in susceptibility to atherosclerosis. The activity of the arterial enzyme was significantly higher in the atherosclerosis-susceptible White Carneau (WC) pigeons than in the resistant Show Racers (SR). The difference was significant whether enzyme activity was calculated on the basis of extract protein, DNA content or fat-free dry weight. In the White Carneau arteries the activity of the enzyme was higher in the female than the male pigeons. PFK is a key regulatory enzyme of glycolysis and is subject to fine control adjustments. A low ATP/ADP ratio and a fall in citrate concentration, as for example, induced by hypoxia, are meditors of a feedback mechanism leading to a rise in PFK activity and enhancement of glycolysis for energy production. This mechanism appears to be the cause of the higher PFK activity in the WC arteries, because related studies indicate impaired Krebs cycle activity in these vessels. It is suggested that the increased dependence of the WC arteries on glycolysis facilitates the development of atherosclerosis in this pigeon strain and that the mechanism is similar to the mechanism by which tissue hypoxia causes lipid accumulation and connective tissue alterations in the arterial wall.
在已知对动脉粥样硬化易感性不同的幼龄(5 - 8周龄)鸽子的动脉中,测定了磷酸果糖激酶(PFK,2.7.1.11)的活性。在易患动脉粥样硬化的白卡诺(WC)鸽中,动脉酶的活性显著高于抗性赛鸽(SR)。无论酶活性是基于提取蛋白、DNA含量还是无脂干重计算,差异均显著。在白卡诺鸽的动脉中,该酶的活性在雌性鸽中高于雄性鸽。PFK是糖酵解的关键调节酶,受到精细的调控。例如,低ATP/ADP比值和因缺氧导致的柠檬酸浓度下降,是一种反馈机制的介质,会导致PFK活性升高以及为产生能量的糖酵解增强。这种机制似乎是WC动脉中PFK活性较高的原因,因为相关研究表明这些血管中的克雷布斯循环活性受损。有人提出,WC动脉对糖酵解的依赖性增加促进了该品系鸽子动脉粥样硬化的发展,并且该机制类似于组织缺氧导致动脉壁脂质积累和结缔组织改变的机制。