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葡萄糖对纯合“糖尿病”(db)突变小鼠胰岛中核糖核酸“体外”合成的影响。

Effects of glucose on the "in vitro" synthesis of ribonucleic acid in pancreatic islets from mice homozygous for the mutation "diabetes" (db).

作者信息

Gunnarsson R

出版信息

Diabete Metab. 1977 Sep;3(3):149-53.

PMID:334588
Abstract

Isolated pancreatic islets obtained from spontaneously diabetic mice were recently shown to have a considerably reduced rate of insulin biosynthesis in response to glucose. This defect has now been further evaluated by in vitro measurements of the effects of glucose on the islet RNA metabolism. An increase of the glucose concentration from 3.3 mM to 16.7 mM more than doubled the incorporation of 3H-labelled uridine into the islet RNA in the normal mice. By contrast, no stimulation was observed in the diabetic mice. Electrophoretic separation, on polyacrylamide gels, of RNA from normal mouse islets indicated that glucose stimulated the incorporation mainly into RNA bigger than 4S. Furthermore the fraction of islet RNA which bound the poly (U) was stimulated in the normal mice but not in the diabetic animals. Taken together these findings indicate a deficient glucose regulation of the RNA metabolism in the diabetic mice which conforms to the previously reported low rate of insulin biosynthesis in response to glucose in these animals.

摘要

最近发现,从自发性糖尿病小鼠分离得到的胰岛对葡萄糖作出反应时,胰岛素生物合成速率显著降低。现在通过体外测量葡萄糖对胰岛RNA代谢的影响,对这一缺陷进行了进一步评估。在正常小鼠中,葡萄糖浓度从3.3 mM增加到16.7 mM,使3H标记的尿苷掺入胰岛RNA的量增加了一倍多。相比之下,在糖尿病小鼠中未观察到刺激作用。对正常小鼠胰岛RNA进行聚丙烯酰胺凝胶电泳分离表明,葡萄糖刺激掺入主要发生在大于4S的RNA中。此外,在正常小鼠中,与聚(U)结合的胰岛RNA部分受到刺激,而在糖尿病动物中则没有。这些发现共同表明,糖尿病小鼠的RNA代谢存在葡萄糖调节缺陷,这与之前报道的这些动物对葡萄糖作出反应时胰岛素生物合成速率较低相一致。

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