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Biochem J. 1968 Jul;108(4):667-73. doi: 10.1042/bj1080667.
2
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本文引用的文献

1
Previous nutritional state and glucose conversion to fatty acids in liver slices.肝脏切片中先前的营养状态及葡萄糖向脂肪酸的转化。
J Biol Chem. 1950 Aug;185(2):845-56.
2
CITRATE AND THE CONVERSION OF CARBOHYDRATE INTO FAT. THE ACTIVITIES OF CITRATE-CLEAVAGE ENZYME AND ACETATE THIOKINASE IN LIVERS OF STARVED AND RE-FED RATS.柠檬酸盐与碳水化合物向脂肪的转化。饥饿和重新喂食大鼠肝脏中柠檬酸裂解酶和乙酸硫激酶的活性。
Biochem J. 1965 Jan;94(1):209-15. doi: 10.1042/bj0940209.
3
METABOLIC CONTROL OF ENZYMES INVOLVED IN LIPOGENESIS AND GLUCONEOGENESIS.脂肪生成和糖异生相关酶的代谢调控
Biochemistry. 1964 Nov;3:1687-92. doi: 10.1021/bi00899a015.
4
MALIC ENZYME AND LIPOGENESIS.苹果酸酶与脂肪生成
Proc Natl Acad Sci U S A. 1964 Nov;52(5):1255-63. doi: 10.1073/pnas.52.5.1255.
5
NICOTINAMIDE ADENINE DINUCLEOTIDE PHOSPHATE-SPECIFIC DEHYDROGENASES IN RELATION TO LIPOGENESIS.与脂肪生成相关的烟酰胺腺嘌呤二核苷酸磷酸特异性脱氢酶
Biochim Biophys Acta. 1964 Jun 15;84:239-50. doi: 10.1016/0926-6542(64)90053-8.
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The hexosemonophosphate shunt and adaptive hyperlipogenesis.磷酸己糖旁路与适应性高脂生成
Diabetes. 1958 Nov-Dec;7(6):478-85. doi: 10.2337/diab.7.6.478.
7
The effect of fasting upon tissue lipogenesis in the intact rat.禁食对完整大鼠组织脂肪生成的影响。
J Biol Chem. 1954 May;208(1):115-22.
8
Metabolic defects in the liver of fasted rats as shown by utilization of C14-labeled glucose and fructose.禁食大鼠肝脏中的代谢缺陷,通过利用C14标记的葡萄糖和果糖得以显示。
J Biol Chem. 1953 Feb;200(2):851-7.
9
Nutritional factors in fatty acid synthesis by tissue slices in vitro.体外组织切片脂肪酸合成中的营养因素。
J Biol Chem. 1952 May;197(1):181-91.
10
Studies on the control of fatty acid synthesis. I. Stimulation by (+)-palmitylcarnitine of fatty acid synthesis in liver preparations from fed and fasted rats.脂肪酸合成调控的研究。I. 喂食及禁食大鼠肝脏制剂中(+)-棕榈酰肉碱对脂肪酸合成的刺激作用。
J Biol Chem. 1967 Mar 10;242(5):865-72.

饥饿以及饥饿后再喂食对生长中雏鸡肝脏中酶活性和[U-14C]葡萄糖代谢的影响。

The effect of starvation and starvation followed by feeding on enzyme activity and the metabolism of [U-14C]glucose in liver from growing chicks.

作者信息

Goodridge A G

出版信息

Biochem J. 1968 Jul;108(4):667-73. doi: 10.1042/bj1080667.

DOI:10.1042/bj1080667
PMID:5667280
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC1198866/
Abstract
  1. The conversion of [U-(14)C]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-(14)C]glucose and the activity of ;malic' enzyme did not increase unless the birds were fed. The response to feeding of [U-(14)C]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-(14)C]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.
摘要
  1. 测定了饥饿或先饥饿后喂食的雏鸡肝脏切片中[U-(14)C]葡萄糖向二氧化碳、胆固醇和脂肪酸的转化,以及肝脏匀浆可溶性部分中“苹果酸”酶、柠檬酸裂解酶、NADP连接的异柠檬酸脱氢酶和磷酸己糖途径脱氢酶的活性。2. 在刚孵出的雏鸡中,除非喂食,[U-(14)C]葡萄糖的掺入和“苹果酸”酶的活性不会增加。随着饥饿雏鸡年龄的增长,其对喂食后[U-(14)C]葡萄糖掺入脂肪酸的反应增强。3. 即使刚孵出的雏鸡未喂食,柠檬酸裂解酶活性也会缓慢增加。喂食后,柠檬酸裂解酶活性增加得更快。4. 在正常喂食的20日龄雏鸡中,饥饿会降低[U-(14)C]葡萄糖向所有三种终产物的掺入,并降低“苹果酸”酶和柠檬酸裂解酶的活性。重新喂食会使所有这些过程增加到正常或高于正常水平。5. 在刚孵出和20日龄的雏鸡中,饥饿都会增加异柠檬酸脱氢酶的活性,而喂食或重新喂食则会降低该活性。6. 在饮食操作过程中,磷酸己糖途径脱氢酶活性几乎没有变化。7. 结果表明,底物向肝脏输送的增加是刚孵出雏鸡中观察到的葡萄糖代谢速率增加的主要刺激因素。结果还表明,“苹果酸”酶和柠檬酸裂解酶活性的变化是代谢物通过葡萄糖-脂肪酸途径流量增加的继发结果,并且磷酸己糖途径的脱氢酶在脂肪酸合成的NADPH产生中起次要作用。