Zara V, Gnoni G V
Department of Biology, University of Lecce, Italy.
Biochim Biophys Acta. 1995 Oct 4;1239(1):33-8. doi: 10.1016/0005-2736(95)00125-m.
The effect of starvation on the activity of the tricarboxylate carrier has been investigated in intact rat liver mitochondria and in a reconstituted system. In both experimental conditions, the rate of citrate transport, when compared to control, is greatly reduced (35-40%) in starved rats. Similar behaviour is shown by the cytosolic lipogenic enzymes. Kinetic analysis of the carrier activity in intact mitochondria and in the proteoliposomal system has showed that during starvation only the Vmax of this process decreases while there is no change in the Km. No difference in the Arrhenius plot and in the lipid composition has been detected, which indicates that the reduced transport activity in fasted animals is not due to a change in the carrier lipid microenvironment. In starved rats, a reduction of the carrier activity has occurred even after the addition of increasing cardiolipin concentrations to proteoliposomes. These findings thus suggest that starvation-induced decrease of citrate carrier activity could be due to a change of the intrinsic properties of the transport protein.
在完整的大鼠肝脏线粒体和重构系统中,研究了饥饿对三羧酸载体活性的影响。在这两种实验条件下,与对照组相比,饥饿大鼠的柠檬酸转运速率大幅降低(35 - 40%)。胞质脂肪生成酶也表现出类似的行为。对完整线粒体和蛋白脂质体系统中载体活性的动力学分析表明,饥饿期间该过程仅Vmax降低,而Km没有变化。在阿累尼乌斯图和脂质组成方面未检测到差异,这表明禁食动物中转运活性的降低并非由于载体脂质微环境的变化。在饥饿大鼠中,即使向蛋白脂质体中添加不断增加浓度的心磷脂后,载体活性仍会降低。因此,这些发现表明饥饿诱导的柠檬酸载体活性降低可能是由于转运蛋白内在特性的改变。