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自发性糖尿病大鼠、丙酮处理大鼠和饥饿大鼠中胆红素UDP-葡萄糖醛酸基转移酶诱导的分子基础。

Molecular basis of bilirubin UDP-glucuronosyltransferase induction in spontaneously diabetic rats, acetone-treated rats and starved rats.

作者信息

Braun L, Coffey M J, Puskás F, Kardon T, Nagy G, Conley A A, Burchell B, Mandl J

机构信息

Department of Medical Chemistry, Semmelweis University of Medicine, P.O. Box 260, H-1444 Budapest, Hungary.

出版信息

Biochem J. 1998 Dec 15;336 ( Pt 3)(Pt 3):587-92. doi: 10.1042/bj3360587.

DOI:10.1042/bj3360587
PMID:9841869
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC1219908/
Abstract

The co-ordinated induction of several hepatic drug-metabolizing enzymes is a common feature in the regulation of drug biotransformation under normal and pathological conditions. In the present study the activity and expression of bilirubin UDP-glucuronosyltransferase (UGT1A1) were investigated in livers of BioBreeding/Worcester diabetic, fasted and acetone-treated rats. Bilirubin glucuronidation was stimulated by all three treatments; this was correlated with an increase in the UGT1A1 protein concentration in hepatic microsomes. Transcriptional induction of UGT1A1 was also observed in diabetes and starvation but not with acetone treatment, which apparently caused translational stabilization of the enzyme protein. The hormonal/metabolic alterations in diabetes and starvation might be a model for postnatal development. The sudden interruption of maternal glucose supply signals the enhanced expression of UGT1A1, giving a novel explanation for the physiological induction of bilirubin glucuronidation in newborn infants.

摘要

在正常和病理条件下，几种肝脏药物代谢酶的协同诱导是药物生物转化调节的一个共同特征。在本研究中，对BioBreeding/Worcester糖尿病大鼠、禁食大鼠和丙酮处理大鼠的肝脏中胆红素UDP-葡萄糖醛酸基转移酶（UGT1A1）的活性和表达进行了研究。所有三种处理均刺激了胆红素葡萄糖醛酸化；这与肝微粒体中UGT1A1蛋白浓度的增加相关。在糖尿病和饥饿状态下也观察到了UGT1A1的转录诱导，但丙酮处理未观察到，丙酮处理显然导致了该酶蛋白的翻译稳定性。糖尿病和饥饿状态下的激素/代谢改变可能是出生后发育的一个模型。母体葡萄糖供应的突然中断标志着UGT1A1表达增强，这为新生儿胆红素葡萄糖醛酸化的生理诱导提供了一种新的解释。

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