Del Villar E, Vega P, Gaule C, Sanchez E
Department of Biochemistry Faculty of Medicine, University of Chile, Santiago.
Eur J Drug Metab Pharmacokinet. 1990 Oct-Dec;15(4):279-85. doi: 10.1007/BF03190216.
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.
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。
