Carter T C, Ramdath D D, Coore H G
Biochemistry Department, Faculty of Medical Sciences, University of the West Indies, Trinidad, WI, USA.
Mol Cell Biochem. 1996 Sep 20;162(2):127-31. doi: 10.1007/BF00227539.
Kinetic behaviour of rat heart pyruvate dehydrogenase kinase (PDHK alpha) was studied in the multi-enzyme complex (PDC) contained in two preparations: mitochondria (mPDC) and a high speed pellet of Triton-extracted tissue (hPDC). Two parameters were evaluated: Vav, related to Vmax, and Fractional Pyruvate Inhibition (FPI). Starvation of rats for 48 h led to a rise in Vav and a fall in FPI. Injection into starved rats of agents which reduce beta-oxidation of fatty acids restored, in succession, FPI and then Vav, of hPDC, to levels found in hPDC from fed animals. In vitro incubation at 30 degrees C of hPDC from starved animals restored FPI, but not Vav to 'fed' values; both were restored during in vitro incubation of mPDC from starved animals within the same time frame as in the in vivo experiments. A sharp increase of FPI, but not Vav, of hPDC from both fed and starved rats was observed in later experiments. This could have been due to differential selection of the two genes for isoenzymes of PDHK alpha proposed by other workers.
在两种制剂中的多酶复合物（PDC）中研究了大鼠心脏丙酮酸脱氢酶激酶（PDHKα）的动力学行为，这两种制剂分别是线粒体（mPDC）和经Triton处理的组织高速沉淀（hPDC）。评估了两个参数：与Vmax相关的Vav和丙酮酸抑制分数（FPI）。大鼠饥饿48小时导致hPDC的Vav升高和FPI降低。向饥饿大鼠注射减少脂肪酸β氧化的药物后，hPDC的FPI和随后的Vav依次恢复到喂食动物的hPDC中发现的水平。饥饿动物的hPDC在30℃下体外孵育可恢复FPI，但不能将Vav恢复到“喂食”值；饥饿动物的mPDC在体外孵育期间，FPI和Vav均在与体内实验相同的时间范围内恢复到“喂食”值。在随后的实验中，观察到喂食和饥饿大鼠的hPDC的FPI急剧增加，但Vav没有增加。这可能是由于其他研究人员提出的PDHKα同工酶的两个基因的差异选择所致。
