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The effect of starvation and starvation followed by feeding on enzyme activity and the metabolism of U-14Cglucose in liver from growing chicks

机译:饥饿和饥饿后进食对生长中的雏鸡肝脏酶活性和U-14C葡萄糖代谢的影响

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摘要

1. The conversion of [U-14C]glucose into carbon dioxide, cholesterol and fatty acids in liver slices and the activities of `malic' enzyme, citrate-cleavage enzyme, NADP-linked isocitrate dehydrogenase and hexose monophosphate-shunt dehydrogenases in the soluble fraction of homogenates of liver were measured in chicks that were starved or starved then fed. 2. In newly hatched chicks the incorporation of [U-14C]glucose and the activity of `malic' enzyme did not increase unless the birds were fed. The response to feeding of [U-14C]glucose incorporation into fatty acids increased as the starved chicks grew older. 3. Citrate-cleavage enzyme activity increased slowly even when the newly hatched chicks were unfed. On feeding, citrate-cleavage enzyme activity increased at a much faster rate. 4. In normally fed 20-day-old chicks starvation decreased the incorporation of [U-14C]glucose into all three end products and depressed the activities of `malic' enzyme and citrate-cleavage enzyme. Re-feeding increased all of these processes to normal or higher-than-normal levels. 5. In both newly hatched and 20-day-old chicks starvation increased the activity of isocitrate dehydrogenase and feeding or re-feeding decreased it. 6. Very little change in hexose monophosphate-shunt dehydrogenase activity was observed during the dietary manipulations. 7. The results indicate that increased substrate delivery to the liver is the principal stimulus to the increased rate of glucose metabolism observed in newly hatched chicks. The results also suggest that changes in the activities of `malic' enzyme and citrate-cleavage enzyme are secondary to an increased flow of metabolites through the glucose-to-fatty acid pathway and that the dehydrogenases of the hexose monophosphate shunt play a minor role in NADPH production for fatty acid synthesis.
机译:1. [U- 14 C]葡萄糖在肝片中的转化为二氧化碳,胆固醇和脂肪酸以及“苹果酸”酶,柠檬酸裂解酶,NADP连接的异柠檬酸脱氢酶和在饥饿或饥饿然后进食的雏鸡中测量肝脏匀浆可溶部分中的己糖单磷酸分流脱氢酶。 2.在新孵出的雏鸡中,除非喂饲,否则[U- 14 C]葡萄糖的掺入和“苹果酸”酶的活性不会增加。随着饥饿的雏鸡年龄的增长,对[U- 14 C]葡萄糖掺入脂肪酸的饲喂反应增加。 3.即使不喂食新孵化的雏鸡,柠檬酸盐切割酶的活性也缓慢增加。进食时,柠檬酸盐切割酶活性以更快的速度增加。 4.在正常喂养的20天大的雏鸡中,饥饿会降低[U- 14 C]葡萄糖在所有三个终产物中的掺入,并降低“苹果酸”酶和柠檬酸裂解酶的活性。重新喂食将所有这些过程提高到正常水平或高于正常水平。 5.在新孵出的雏鸡和20天大的雏鸡中,饥饿都增加了异柠檬酸脱氢酶的活性,而饲喂或再饲喂则降低了它的活性。 6.在饮食操作过程中,己糖一磷酸分流脱氢酶活性几乎没有变化。 7.结果表明,增加向肝脏的底物传递是新孵化雏鸡中观察到的葡萄糖代谢率增加的主要刺激因素。结果还表明,“苹果酸”酶和柠檬酸裂解酶的活性变化是通过葡萄糖到脂肪酸途径的代谢物流量增加所引起的,而己糖一磷酸分流器的脱氢酶在NADPH生产用于脂肪酸合成。

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