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链脲佐菌素诱导的糖尿病大鼠肝脏微粒体葡萄糖-6-磷酸酶蛋白水平升高。

Rat hepatic microsomal glucose-6-phosphatase protein levels are increased in streptozotocin-induced diabetes.

作者信息

Burchell A, Cain D I

出版信息

Diabetologia. 1985 Nov;28(11):852-6. doi: 10.1007/BF00291077.

DOI:10.1007/BF00291077
PMID:3002890
Abstract

Hepatic microsomal glucose-6-phosphatase activity levels and the hepatic output of glucose are increased in diabetes. We have used protein chemistry and immunological techniques to determine the mechanism by which the activity levels of the glucose-6-phosphatase system are increased in streptozotocin-induced diabetic rats. In the streptozotocin-induced diabetic rats, the activity of the glucose-6-phosphatase enzyme increased four-fold without appreciably altering the transport capacity of the glucose-6-phosphatase system. The solubilized diabetic rat liver glucose-6-phosphatase enzyme appeared to be very similar to the solubilized enzyme from control rat liver microsomes. They exhibit the same Km, are labile at 30 degrees C, are stabilized by sodium fluoride and they migrate to the same position during density gradient centrifugation. Immunological studies demonstrated that a greater amount of hepatic microsomal glucose-6-phosphatase enzyme protein is present in diabetic rats than in control rats. Thus, we have determined for the first time that increased levels of the glucose-6-phosphatase protein are present in streptozotocin-induced diabetes. The significance of this finding in relation to the regulation of the hepatic microsomal glucose-6-phosphatase system is discussed.

摘要

糖尿病时肝脏微粒体葡萄糖-6-磷酸酶活性水平及肝脏葡萄糖输出增加。我们运用蛋白质化学和免疫学技术来确定链脲佐菌素诱导的糖尿病大鼠中葡萄糖-6-磷酸酶系统活性水平升高的机制。在链脲佐菌素诱导的糖尿病大鼠中,葡萄糖-6-磷酸酶的活性增加了四倍,而葡萄糖-6-磷酸酶系统的转运能力没有明显改变。溶解的糖尿病大鼠肝脏葡萄糖-6-磷酸酶似乎与对照大鼠肝脏微粒体中的溶解酶非常相似。它们具有相同的米氏常数,在30℃时不稳定,可被氟化钠稳定,并且在密度梯度离心过程中迁移到相同位置。免疫学研究表明,糖尿病大鼠肝脏微粒体中葡萄糖-6-磷酸酶蛋白的含量高于对照大鼠。因此,我们首次确定链脲佐菌素诱导的糖尿病中葡萄糖-6-磷酸酶蛋白水平升高。讨论了这一发现与肝脏微粒体葡萄糖-6-磷酸酶系统调节的关系。

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1
Rat hepatic microsomal glucose-6-phosphatase protein levels are increased in streptozotocin-induced diabetes.链脲佐菌素诱导的糖尿病大鼠肝脏微粒体葡萄糖-6-磷酸酶蛋白水平升高。
Diabetologia. 1985 Nov;28(11):852-6. doi: 10.1007/BF00291077.
2
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3
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5
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6
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Diabetes. 1979 Jul;28(7):664-79. doi: 10.2337/diab.28.7.664.
8
The phosphohydrolase component of the hepatic microsomal glucose-6-phosphatase system is a 36.5-kilodalton polypeptide.肝脏微粒体葡萄糖-6-磷酸酶系统的磷酸水解酶成分是一种36.5千道尔顿的多肽。
J Biol Chem. 1988 Feb 25;263(6):2673-8.
9
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Biochem Soc Trans. 1992 Aug;20(3):271S. doi: 10.1042/bst020271s.
10
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Biochem J. 1977 Nov 15;168(2):147-53. doi: 10.1042/bj1680147.

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LIVER MICROSOMAL GLUCOSE 6-PHOSPHATASE, INORGANIC PYROPHOSPHATASE, AND PYROPHOSPHATE-GLUCOSE PHOSPHOTRANSFERASE. 3. ASSOCIATED NUCLEOSIDE TRIPHOSPHATE- AND NUCLEOSIDE DIPHOSPHATE-GLUCOSE PHOSPHOTRANSFERASE ACTIVITIES.肝脏微粒体葡萄糖6-磷酸酶、无机焦磷酸酶和焦磷酸-葡萄糖磷酸转移酶。3. 相关的核苷三磷酸和核苷二磷酸-葡萄糖磷酸转移酶活性
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哺乳期和断乳期灰海豹幼崽的肝脏葡萄糖-6-磷酸酶蛋白:与其他哺乳动物的结构相似性及其与营养、胰岛素信号和代谢物水平的关系。
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Fasting hyperglycemia is not associated with increased expression of PEPCK or G6Pc in patients with Type 2 Diabetes.在2型糖尿病患者中,空腹血糖升高与磷酸烯醇式丙酮酸羧激酶(PEPCK)或葡萄糖-6-磷酸酶(G6Pc)表达增加无关。
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Oral tungstate treatment improves only transiently alteration of glucose metabolism in a new rat model of type 2 diabetes.在一种新的2型糖尿病大鼠模型中,口服钨酸盐治疗仅能短暂改善葡萄糖代谢的改变。
Endocrine. 2002 Nov;19(2):177-84. doi: 10.1385/ENDO:19:2:177.
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Histone 2A stimulates glucose-6-phosphatase activity by permeabilization of liver microsomes.组蛋白2A通过使肝微粒体通透化来刺激葡萄糖-6-磷酸酶活性。
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Therapeutic insulin and hepatic glucose-6-phosphatase activity in preterm infants.早产婴儿的治疗性胰岛素与肝脏葡萄糖-6-磷酸酶活性
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Hepatocyte nuclear factor-1 acts as an accessory factor to enhance the inhibitory action of insulin on mouse glucose-6-phosphatase gene transcription.肝细胞核因子-1作为一种辅助因子,可增强胰岛素对小鼠葡萄糖-6-磷酸酶基因转录的抑制作用。
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The glucose-6-phosphatase enzyme in developing human trachea and oesophagus.发育中的人类气管和食管中的葡萄糖-6-磷酸酶
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Differential time course of liver and kidney glucose-6 phosphatase activity during long-term fasting in rat correlates with differential time course of messenger RNA level.大鼠长期禁食期间肝脏和肾脏葡萄糖-6-磷酸酶活性的差异时间进程与信使核糖核酸水平的差异时间进程相关。
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Glycogen storage disease type Ib.Ⅰb型糖原贮积病
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Type Ic, a novel glycogenosis. Underlying mechanism.Ic型,一种新型糖原贮积病。潜在机制。
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Identification and purification of a liver microsomal glucose 6-phosphatase.肝微粒体葡萄糖6-磷酸酶的鉴定与纯化
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The importance of membrane integrity in kinetic characterizations of the microsomal glucose-6-phosphatase system.膜完整性在微粒体葡萄糖-6-磷酸酶系统动力学特性研究中的重要性。
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Evidence for the participation of independent translocation for phosphate and glucose 6-phosphate in the microsomal glucose-6-phosphatase system. Interactions of the system with orthophosphate, inorganic pyrophosphate, and carbamyl phosphate.微粒体葡萄糖-6-磷酸酶系统中磷酸和6-磷酸葡萄糖独立转运参与的证据。该系统与正磷酸盐、无机焦磷酸盐和氨基甲酰磷酸盐的相互作用。
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Stabilization of partially-purified glucose 6-phosphatase by fluoride. Is enzyme inactivation caused by dephosphorylation?氟化物对部分纯化的葡萄糖6-磷酸酶的稳定作用。酶失活是由去磷酸化引起的吗?
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Type Ib glycogen storage disease is caused by a defect in the glucose-6-phosphate translocase of the microsomal glucose-6-phosphatase system.I型糖原贮积病是由微粒体葡萄糖-6-磷酸酶系统的葡萄糖-6-磷酸转运酶缺陷引起的。
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