GLYCYRRHETINIC ACID, AN INHIBITOR OF 11-BETA-HYDROXYSTEROID DEHYDROGENASE, ALTERS LOCAL CEREBRAL GLUCOSE-UTILIZATION INVIVO

被引：24

作者：

SECKL, JR ^{[1
]}

KELLY, PAT ^{[1
]}

SHARKEY, J ^{[1
]}

机构：

[1] UNIV EDINBURGH,WESTERN GEN HOSP,DEPT CLIN NEUROSCI,EDINBURGH EH4 2XU,SCOTLAND

来源：

JOURNAL OF STEROID BIOCHEMISTRY AND MOLECULAR BIOLOGY | 1991年 / 39卷 / 5A期

基金：

英国惠康基金;

关键词：

D O I：

10.1016/0960-0760(91)90379-J

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

11-beta-Hydroxysteroid dehydrogenase (11-beta-OHSD) metabolizes corticosterone (B) to inactive 11-dehydrocorticosterone and thus protects the non-specific renal mineralocorticoid receptor from exposure to B in vivo. There is regional 11-beta-OHSD mRNA expression and bioactivity in brain in vitro, but any in vivo function is unknown. We used the [C-14]2-deoxyglucose technique in conscious rats to investigate whether 11-beta-OHSD inhibition with glycyrrhetinic acid alters local cerebral metabolic activity. We found increased glucose use in subregions of the hypothalamus, hippocampus, neocortex and subthalamus. Thus, 11-beta-OHSD may play a role in regulating the effects of B in the brain, in vivo.

引用

页码：777 / 779

页数：3

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