EFFECT OF URSODEOXYCHOLIC ACID ON HEPATIC CHOLESTEROL-METABOLISM
EFFECT OF URSODEOXYCHOLIC ACID ON HEPATIC CHOLESTEROL-METABOLISM
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DOI：
10.3109/00365529409103620
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发表时间：
1994-01-01
影响因子：
1.9
通讯作者：
EINARSSON, K
中科院分区：
文献类型：
--
作者：
EINARSSON, K
口服熊去氧胆酸（UDCA）通过减少胆固醇的肝脏输出使胆汁不饱和胆固醇。从理论上讲，有几种机制可能很重要。在本综述中，评估了UDCA治疗对肝脏胆固醇代谢的影响，特别是对肝脏胆固醇合成、3-羟基-3-甲基戊二酰辅酶A （HMG CoA）还原酶活性、胆汁酸合成、胆固醇7 α -羟基化和胆固醇酰基辅酶A的酯化：胆固醇乙酰转移酶（ACAT）活性的影响。很明显，UDCA治疗不抑制肝脏HMG CoA还原酶活性。UDCA对ACAT活性和胆固醇酯含量也没有影响。在使用UDCA期间，胆固醇对胆汁酸的分解代谢不受影响或略有增加。由此得出的结论是，受刺激的胆固醇降解为胆汁酸可能部分解释了UDCA给药期间肝脏胆固醇分泌减少的原因。这表明，在UDCA治疗期间，肠道胆固醇吸收的减少也可能是重要的。
Oral administration of ursodeoxycholic acid (UDCA) renders bile unsaturated with cholesterol by reducing the hepatic output of cholesterol. Theoretically, several mechanisms may be of importance. In the present overview, the effect of treatment with UDCA on hepatic cholesterol metabolism is evaluated, in particular the influence on hepatic cholesterol synthesis, 3-hydroxy-3-methylglutaryl coenzyme A (HMG CoA) reductase activity, bile acid synthesis, 7 alpha-hydroxylation of cholesterol, and esterification of cholesterol-acyl coenzyme A: cholesterol acetyltransferase (ACAT) activity. It is apparent that UDCA treatment does not inhibit the hepatic HMG CoA reductase activity. Neither is ACAT activity or the cholesteryl ester content changed by UDCA. The catabolism of cholesterol to bile acids is unaffected or slightly increased during administration of UDCA. It is concluded that a stimulated degradation of cholesterol to bile acids may partly explain the decrease in hepatic secretion of cholesterol obtained during UDCA administration. It is suggested that the reduction in cholesterol absorption from the intestine seen during UDCA therapy may also be of importance.