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糖原贮积病(gsd/gsd)大鼠肝脏组织中磷酸化酶b激酶与年龄相关的增加

Age-related augmentation of phosphorylase b kinase in hepatic tissue from the glycogen-storage-disease (gsd/gsd) rat.

作者信息

Clark D G, Neville S D, Brinkman M, Nelson P V, Illman R J, Guthberlet A, Haynes W D

出版信息

Biochem J. 1986 Sep 15;238(3):811-6. doi: 10.1042/bj2380811.

DOI:10.1042/bj2380811
PMID:3099776
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC1147208/
Abstract

The effects of food deprivation on body weight, liver weight, hepatic glycogen content, glycogenolytic enzymes and blood metabolites were compared in young and old phosphorylase b kinase-deficient (gsd/gsd) rats. Although the concentration of glycogen in liver from 9-week-old female gsd/gsd rats (730 mumol of glucose equivalents/g wet wt.) was increased by 7-8% during starvation, total hepatic glycogen was decreased by 12% after 24 h without food. In 12-month-old male gsd/gsd rats the concentration of liver glycogen (585 mumol of glucose equiv./g wet wt.) was decreased by 16% and total hepatic glycogen by nearly 40% after food deprivation for 24 h. Phosphorylase b kinase and phosphorylase a were present at approx. 10% of the control activities in 9-week-old gsd/gsd rats, but both enzyme activities were increased more than 3-fold in 12-month-old affected rodents. It is concluded that the age-related ability to mobilize hepatic glycogen appears to result from the augmentation of phosphorylase b kinase during maturation of the gsd/gsd rat.

摘要

在年轻和年老的磷酸化酶b激酶缺陷(gsd/gsd)大鼠中,比较了食物剥夺对体重、肝脏重量、肝糖原含量、糖原分解酶和血液代谢物的影响。尽管9周龄雌性gsd/gsd大鼠肝脏中的糖原浓度(730微摩尔葡萄糖当量/克湿重)在饥饿期间增加了7-8%,但在禁食24小时后,肝脏总糖原减少了12%。在12月龄雄性gsd/gsd大鼠中,禁食24小时后,肝糖原浓度(585微摩尔葡萄糖当量/克湿重)降低了16%,肝脏总糖原降低了近40%。在9周龄的gsd/gsd大鼠中,磷酸化酶b激酶和磷酸化酶a的活性约为对照活性的10%,但在12月龄的患病啮齿动物中,这两种酶的活性均增加了3倍以上。得出的结论是,gsd/gsd大鼠成熟过程中磷酸化酶b激酶的增加似乎导致了与年龄相关的肝糖原动员能力。

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1
Age-related augmentation of phosphorylase b kinase in hepatic tissue from the glycogen-storage-disease (gsd/gsd) rat.糖原贮积病(gsd/gsd)大鼠肝脏组织中磷酸化酶b激酶与年龄相关的增加
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引用本文的文献

1
Suppression of hepatic glucose output after glucose re-feeding in the gsd/gsd rat.gsd/gsd大鼠重新喂食葡萄糖后肝脏葡萄糖输出的抑制
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2
Starvation of phosphorylase kinase deficient rats is accompanied by partial hepatic glycogen depletion.磷酸化酶激酶缺陷型大鼠饥饿时伴有部分肝糖原消耗。
Biochem J. 1988 Jun 15;252(3):927-8. doi: 10.1042/bj2520927.
3
The hepatic glycogenolysis induced by reversible ischaemia or KCN is exclusively catalysed by phosphorylase a.由可逆性缺血或氰化钾诱导的肝糖原分解完全由磷酸化酶a催化。
Biochem J. 1988 Dec 1;256(2):685-8. doi: 10.1042/bj2560685.

本文引用的文献

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Protein measurement with the Folin phenol reagent.使用福林酚试剂进行蛋白质测定。
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Glucose homeostasis during the perinatal period in normal rats and rats with a glycogen storage disorder.正常大鼠和患有糖原贮积症的大鼠围产期的葡萄糖稳态。
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Glycogen metabolism in the liver of the neonatal gsd/gsd and control (GSD/GSD) rat.新生糖原贮积病/糖原贮积病大鼠和对照(GSD/GSD)大鼠肝脏中的糖原代谢
Biochem J. 1982 Mar 15;202(3):623-9. doi: 10.1042/bj2020623.
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Glycogen-storage disease in rats, a genetically determined deficiency of liver phosphorylase kinase.大鼠糖原贮积病,一种由基因决定的肝磷酸化酶激酶缺乏症。
Biochem J. 1980 Apr 15;188(1):99-106. doi: 10.1042/bj1880099.
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A glycogen storage disease (gsd/gsd) rat: studies on lipid metabolism, lipogenesis, plasma metabolites, and bile acid secretion.一种糖原贮积病(gsd/gsd)大鼠:脂质代谢、脂肪生成、血浆代谢物及胆汁酸分泌的研究
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Direction of carbon flux in starvation and after refeeding: in vitro and in vivo effects of 3-mercaptopicolinate.饥饿及再喂养时碳通量的方向:3-巯基吡啶甲酸盐的体外和体内效应
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A glycogen storage disease in rats. Morphological and biochemical investigations.
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Glycogen-storage disease associated with phosphorylase kinase deficiency: evidence for X inactivation.与磷酸化酶激酶缺乏相关的糖原贮积病:X染色体失活的证据。
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