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饥饿和链脲佐菌素诱导糖尿病大鼠肝脏葡萄糖激酶的周转加速

Accelerated turnover of hepatic glucokinase in starved and streptozotocin-diabetic rat.

作者信息

Sibrowski W, Staegemann U, Seitz H J

出版信息

Eur J Biochem. 1982 Oct;127(3):571-4. doi: 10.1111/j.1432-1033.1982.tb06910.x.

Abstract

Rat liver glucokinase synthesis and degradation was estimated in fasted/fed and diabetic/diabetic-insulin-treated rats by the radioimmunological technique. Starvation and Streptozotocin-diabetes led to basal rates of synthesis and, consequently, to low levels in enzyme activity. In addition, a decrease in the apparent half-life from about 19 h in the fed or diabetic-insulin substituted to about 11 h in the starved or diabetic rat, respectively, was observed. Injection of Bt2cAMP into glucose-fed animals reduced glucokinase synthesis to basal levels within 90 min, without affecting enzyme activity. It is concluded that in metabolic states associated with elevated levels in tissue cAMP glucokinase synthesis is reduced to basal values and, in addition, its rate of degradation is significantly enhanced.

摘要

采用放射免疫技术评估禁食/喂食及糖尿病/糖尿病胰岛素治疗大鼠的肝脏葡萄糖激酶合成与降解情况。饥饿和链脲佐菌素诱导的糖尿病导致基础合成速率下降,进而酶活性水平降低。此外,观察到表观半衰期从喂食或糖尿病胰岛素替代大鼠的约19小时分别降至饥饿或糖尿病大鼠的约11小时。向喂食葡萄糖的动物注射Bt2cAMP可在90分钟内将葡萄糖激酶合成降至基础水平,而不影响酶活性。得出的结论是,在与组织cAMP水平升高相关的代谢状态下,葡萄糖激酶合成降至基础值,此外,其降解速率显著加快。

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