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磷酸烯醇丙酮酸羧激酶在大鼠肝和脂肪组织中的合成与降解。饥饿-再喂养循环期间的变化。

Synthesis and degradation of phosphoenolpyruvate carboxylase in rat liver and adipose tissue. Changes during a starvation-re-feeding cycle.

机构信息

Commonwealth Scientific and Industrial Research Organization, Division of Nutritional Biochemistry, Adelaide, S. Austral. 5000, Australia.

出版信息

Biochem J. 1973 Jun;134(2):445-53. doi: 10.1042/bj1340445.

DOI:10.1042/bj1340445
PMID:16742804
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC1177830/
Abstract

A specific antibody against liver cytosol phosphoenolpyruvate carboxylase (EC 4.1.1.32) was used to isolate the enzyme from liver and adipose tissue. With this technique we have shown that phosphoenolpyruvate carboxylase synthesis in starved rats accounts for 3% of the total synthesis of cytosol protein in each tissue. Re-feeding starved animals decreases this relative rate of phosphoenolpyruvate carboxylase synthesis to 0.2% and 1% respectively in liver and adipose tissue, and the activity of the enzyme in each tissue is decreased to 25% of the starvation value. An additional starvation period is accompanied by an increased rate of enzyme synthesis, but the response to starvation is considerably slower than that caused by re-feeding. The degradation rate of phosphoenolpyruvate carboxylase is also subject to regulation. Thus re-feeding starved animals decreases the half-life of the enzyme in liver from 13h to 5.2h, but the rapid rate of degradation is maintained at least during the first 20h of subsequent starvation. Only slight changes in the degradation rate of phosphoenolpyruvate carboxylase are found in adipose tissue. We conclude that the large alterations in the rate of enzyme synthesis during a starvation-re-feeding cycle are the major cause of fluctuations in activity.

摘要

一种针对肝胞质磷酸烯醇丙酮酸羧激酶(EC 4.1.1.32)的特异性抗体被用于从肝脏和脂肪组织中分离该酶。通过这项技术,我们发现禁食大鼠肝和脂肪组织中磷酸烯醇丙酮酸羧激酶的合成量分别占胞质蛋白总合成量的 3%和 1%。重新喂食饥饿的动物会使肝和脂肪组织中磷酸烯醇丙酮酸羧激酶的相对合成率分别降低至 0.2%和 1%,且每个组织中酶的活性也降低至饥饿值的 25%。再次饥饿会导致酶合成率增加,但对饥饿的反应速度明显比重新喂食慢。磷酸烯醇丙酮酸羧激酶的降解率也受到调节。因此,重新喂食饥饿的动物会使肝中酶的半衰期从 13 小时缩短至 5.2 小时,但在随后的至少 20 小时的饥饿期内,仍能维持快速降解速度。在脂肪组织中,磷酸烯醇丙酮酸羧激酶的降解率仅发生轻微变化。我们的结论是,在饥饿-重新喂食循环中,酶合成率的大幅变化是活性波动的主要原因。

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