Suppr超能文献

雌性大鼠的糖尿病;肝脏微粒体氨基比林N-脱甲基酶和UDP-葡萄糖醛酸基转移酶活性的变化

Diabetes in female rats; changes in liver microsomal aminopyrine N-demethylase and UDP-glucuronyl transferase activities.

作者信息

Del Villar E, Vega P, Gaule C, Sanchez E

机构信息

Department of Biochemistry Faculty of Medicine, University of Chile, Santiago.

出版信息

Eur J Drug Metab Pharmacokinet. 1990 Oct-Dec;15(4):279-85. doi: 10.1007/BF03190216.

Abstract

Short or long term diabetes in female rats produced remarkable activation of aminopyrine N-demethylation, inhibition of oestrone and p-nitrophenol glucuronidation and no changes in morphine UDP-glucuronyltransferase activity in vitro. Km and Vmax for these reactions were determined. Insulin treatment partially antagonized diabetes activation of aminopyrine N-demethylation: it restored decreased UDP-glucuronyltransferase activities for oestrone and p-nitrophenol only in long term and short term diabetes, respectively. Insulin also markedly inhibited morphine glucuronidation. Triton X-100 also displayed a differential pattern of activation for the glucuronidation reactions in liver microsomes of diabetic rats. Results suggest that diabetes in female rats may increase the actual amount of enzyme protein for aminopyrine metabolism and to decrease that for oestrone and p-nitrophenol.

摘要

雌性大鼠的短期或长期糖尿病在体外显著激活了氨基比林N-脱甲基化,抑制了雌酮和对硝基苯酚葡萄糖醛酸化,且吗啡UDP-葡萄糖醛酸基转移酶活性无变化。测定了这些反应的米氏常数(Km)和最大反应速度(Vmax)。胰岛素治疗部分拮抗了糖尿病对氨基比林N-脱甲基化的激活作用:它仅分别在长期和短期糖尿病中恢复了雌酮和对硝基苯酚降低的UDP-葡萄糖醛酸基转移酶活性。胰岛素还显著抑制了吗啡葡萄糖醛酸化。曲拉通X-100对糖尿病大鼠肝微粒体中的葡萄糖醛酸化反应也表现出不同的激活模式。结果表明,雌性大鼠的糖尿病可能会增加氨基比林代谢的酶蛋白实际量,并减少雌酮和对硝基苯酚的酶蛋白量。

文献AI研究员

20分钟写一篇综述,助力文献阅读效率提升50倍。

立即体验

用中文搜PubMed

大模型驱动的PubMed中文搜索引擎

马上搜索

文档翻译

学术文献翻译模型,支持多种主流文档格式。

立即体验