Hall R, Kok E, Javitt N B
Division of Hepatic Diseases, New York University Medical Center, New York 10016.
FASEB J. 1988 Feb;2(2):152-6. doi: 10.1096/fasebj.2.2.3342968.
The regulation of bile acid synthesis was studied in rabbits after interruption of the enterohepatic circulation by choledochoureteral anastomosis. Total daily bile acid output was 772 +/- 130 (SD) mumol/24 h, of which greater than 95% was glycocholic acid. Administration of deoxycholic or cholic acid or their conjugates (300-800 mumol) or gall-bladder bile failed to down-regulate endogenous bile acid synthesis. In contrast, chenodeoxycholic acid administration did down-regulate bile acid synthesis, but this effect was related to the formation and excretion of lithocholic acid. This observation was confirmed by the finding that i.v. infusion of 10-20 mumol of either lithocholic acid or 3 beta-hydroxy-5-cholenoic acid significantly reduced cholic acid synthesis. Thus monohydroxy bile acids, derived from either hepatic or intestinal sources, participate in the down-regulation of bile acid synthesis.
通过胆总管输尿管吻合术中断肠肝循环后,对家兔胆汁酸合成的调节进行了研究。每日胆汁酸总排出量为772±130(标准差)μmol/24小时,其中超过95%为甘氨胆酸。给予脱氧胆酸或胆酸及其共轭物(300 - 800μmol)或胆囊胆汁未能下调内源性胆汁酸合成。相反,给予鹅去氧胆酸确实下调了胆汁酸合成,但这种作用与石胆酸的形成和排泄有关。静脉输注10 - 20μmol石胆酸或3β - 羟基 - 5 - 胆烯酸可显著降低胆酸合成,这一发现证实了上述观察结果。因此,源自肝脏或肠道的单羟基胆汁酸参与了胆汁酸合成的下调过程。