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四氧嘧啶糖尿病大鼠脑内的蛋白水解活性:脑提取物中存在蛋白水解激活剂。

Proteolytic activity in the brain of alloxan diabetic rats: Presence of a proteolytic activator in the cerebral extract.

机构信息

Al Ameen College of Pharmacy, Hosur Road, Bangalore - 560 027, India.

出版信息

Int J Diabetes Dev Ctries. 2008 Jul;28(3):83-5. doi: 10.4103/0973-3930.44078.

DOI:10.4103/0973-3930.44078
PMID:19902040
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2772018/
Abstract

BACKGROUND AND AIM

Diabetes mellitus is known to cause neurological disorders due to impaired glucose metabolism involving decreased utilization of glucose by the brain tissues. The mechanisms responsible for failure of glycemic regulation in type-2 diabetes leading to neurological impairment need to be thoroughly elucidated.

MATERIALS AND METHODS

Type-2 diabetes was induced in albino rat models with alloxan monohydrate (40 mg/kg i.v.). Cerebral cortex and medulla oblongata were investigated 48 h after alloxan administration for the alterations in proteolytic activity.

RESULTS

Diabetes caused an elevation (P < 0.001) of blood glucose and also proteolytic activity in the brain.

CONCLUSION

Impaired glucose metabolism in the brain was the key factor which was responsible for the elevated (P < 0.001) proteolysis leading to brain dysfunction.

摘要

背景与目的

众所周知,糖尿病会因葡萄糖代谢受损导致神经功能障碍,其中包括脑组织对葡萄糖的利用减少。2型糖尿病患者血糖调节失败导致神经损伤的机制需要深入阐明。

材料与方法

用一水合四氧嘧啶(40mg/kg静脉注射)诱导白化大鼠模型患2型糖尿病。在注射四氧嘧啶48小时后,研究大脑皮层和延髓蛋白水解活性的变化。

结果

糖尿病导致血糖升高(P<0.001),同时大脑中的蛋白水解活性也升高。

结论

大脑中葡萄糖代谢受损是导致蛋白水解增加(P<0.001)进而引起脑功能障碍的关键因素。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/34b3/2772018/585af833a40a/IJDDC-28-83-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/34b3/2772018/585af833a40a/IJDDC-28-83-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/34b3/2772018/585af833a40a/IJDDC-28-83-g001.jpg

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