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[关于口服抗糖尿病药物对体外蛋白质生物合成的影响(作者译)]

[On the influence of oral antidiabetics on protein biosynthesis in vitro (author's transl)].

作者信息

Tragl K H

出版信息

Arzneimittelforschung. 1976;26(3):374-7.

PMID:989329
Abstract

Inhibition of protein synthesis is one of the few side effects of sulfonylureas and biguanides. Regarding our results obtained with hepatic polyribosomes from diabetic and from control animals, with ribosomes directed by polyuridylic acid as a synthetic messenger, and by centrifugation of the ribosomes through sucrose gradients there is evidence of a direct inhibiting effect of tolbutamide on liver ribosomes. The effect of butyl-biguanide depends on the system used for in vitro protein synthesis. While it is inhibiting protein synthesis of normal liver ribosomes regardless of the attached messenger, it stimulates the incorporation of amino acids by ribosomes from diabetic rats directed by endogenous or by synthetic messengers. The specific pattern of ribosomal distribution in sucrose gradients is unchanged by the administration of tolbutamide to the animal prior to its decapitation. However, butyl-biguanide leads to reduction of the polyribosomal portion of liver ribosomes from normal animals while it is without any furhter effect on the amount of polyribosomes already reduced in diabetes mellitus.

摘要

蛋白质合成抑制是磺脲类和双胍类药物为数不多的副作用之一。关于我们用糖尿病动物和对照动物的肝脏多核糖体、以聚尿苷酸作为合成信使指导的核糖体以及通过蔗糖梯度对核糖体进行离心所获得的结果,有证据表明甲苯磺丁脲对肝脏核糖体有直接抑制作用。丁基双胍的作用取决于用于体外蛋白质合成的系统。无论附着的信使如何,它都能抑制正常肝脏核糖体的蛋白质合成,但能刺激糖尿病大鼠核糖体在内源性或合成信使指导下的氨基酸掺入。在动物断头前给予甲苯磺丁脲,蔗糖梯度中核糖体分布的特定模式没有改变。然而,丁基双胍会导致正常动物肝脏核糖体的多核糖体部分减少,而对糖尿病中已经减少的多核糖体数量没有进一步影响。

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