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熊去氧胆酸喂养(无论是否补充牛磺酸)对仓鼠肝脏胆汁酸和胆固醇代谢的影响。

Effect of tauroursodeoxycholate feeding, with or without taurine supplementation on hepatic bile acids and cholesterol metabolism in the hamster.

作者信息

Bellentani S, Bosisio E, Pecorari M, De Fabiani E, Cordoma P, Crestani M, Manenti F

出版信息

Pharmacol Res Commun. 1987 May;19(5):327-39. doi: 10.1016/0031-6989(87)90070-1.

DOI:10.1016/0031-6989(87)90070-1
PMID:3628457
Abstract

This study reports the effect of short-term tauroursodeoxycholic acid (TUDCA) and of TUDCA with addition of taurine on the lipid composition of gallbladder bile, on cholesterol and bile acid synthesis and intestinal excretion, in the female hamsters. After either one or two weeks, the percentage of ursodeoxycholic acid (UDCA) and chenodeoxycholic acid (CDCA) in bile of treated hamsters significantly increased. Both treatments (TUDCA alone or TUDCA + taurine) decreased the percentage of cholic acid without affecting 3-hydroxy-3-methylglutaryl CoA (HMG-CoA) reductase or cholesterol 7 alpha-hydroxylase activities. Sterol and bile acid content of the feces collected during the period of the study did not show any difference. Bile acid glycine to taurine conjugation ratio (G/T ratio) in TUDCA treated animals was significantly higher in respect to controls after only one week of treatment. On the contrary, bile acid G/T ratio significantly decreased in the group of animals supplemented with taurine, but only after two weeks of treatment.

摘要

本研究报告了短期牛磺熊去氧胆酸(TUDCA)以及添加牛磺酸的TUDCA对雌性仓鼠胆囊胆汁脂质成分、胆固醇和胆汁酸合成及肠道排泄的影响。在治疗一周或两周后,接受治疗的仓鼠胆汁中熊去氧胆酸(UDCA)和鹅去氧胆酸(CDCA)的百分比显著增加。两种治疗方法(单独使用TUDCA或TUDCA+牛磺酸)均降低了胆酸的百分比,而不影响3-羟基-3-甲基戊二酰辅酶A(HMG-CoA)还原酶或胆固醇7α-羟化酶的活性。研究期间收集的粪便中固醇和胆汁酸含量没有显示出任何差异。仅在治疗一周后,TUDCA治疗的动物中胆汁酸甘氨酸与牛磺酸的结合率(G/T比)相对于对照组显著更高。相反,补充牛磺酸的动物组中胆汁酸G/T比显著降低,但仅在治疗两周后出现。

相似文献

1
Effect of tauroursodeoxycholate feeding, with or without taurine supplementation on hepatic bile acids and cholesterol metabolism in the hamster.熊去氧胆酸喂养(无论是否补充牛磺酸)对仓鼠肝脏胆汁酸和胆固醇代谢的影响。
Pharmacol Res Commun. 1987 May;19(5):327-39. doi: 10.1016/0031-6989(87)90070-1.
2
Taurine increases bile acid pool size and reduces bile saturation index in the hamster.牛磺酸可增加仓鼠的胆汁酸池大小并降低胆汁饱和指数。
J Lipid Res. 1987 Sep;28(9):1021-7.
3
Hepatic cholesterol and bile acid metabolism in subjects with gallstones: comparative effects of short erm feeding of chenodeoxycholic and ursodeoxycholic acid.胆结石患者的肝脏胆固醇和胆汁酸代谢:短期给予鹅去氧胆酸和熊去氧胆酸的比较效果
J Lipid Res. 1980 Jan;21(1):35-43.
4
Effects of feeding chenodeoxycholic acid on metabolism of cholesterol and bile acids in germ-free rats.饲喂鹅去氧胆酸对无菌大鼠胆固醇和胆汁酸代谢的影响。
Lipids. 1981 Apr;16(4):228-33. doi: 10.1007/BF02535021.
5
Enrichment of bile with tauroursodeoxycholic acid and biliary cholesterol saturation in hamsters.仓鼠中牛磺熊去氧胆酸对胆汁的富集作用及胆汁胆固醇饱和度
Am J Physiol. 1982 Nov;243(5):G424-7. doi: 10.1152/ajpgi.1982.243.5.G424.
6
Taurine ameliorates cholesterol metabolism by stimulating bile acid production in high-cholesterol-fed rats.牛磺酸通过刺激高胆固醇喂养大鼠的胆汁酸生成来改善胆固醇代谢。
Clin Exp Pharmacol Physiol. 2016 Mar;43(3):372-8. doi: 10.1111/1440-1681.12534.
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Regulation of bile acid synthesis. I. Effects of conjugated ursodeoxycholate and cholate on bile acid synthesis in chronic bile fistula rat.胆汁酸合成的调节。I. 结合型熊去氧胆酸和胆酸对慢性胆瘘大鼠胆汁酸合成的影响。
Hepatology. 1988 Mar-Apr;8(2):358-65. doi: 10.1002/hep.1840080228.
8
Early morphologic and enzymatic changes in livers of rats treated with chenodeoxycholic and ursodeoxycholic acids.经鹅去氧胆酸和熊去氧胆酸处理的大鼠肝脏的早期形态学和酶学变化。
Hepatology. 1983 Mar-Apr;3(2):201-8. doi: 10.1002/hep.1840030212.
9
Modeling plasma lipoprotein-bile lipid relationships: differential impact of psyllium and cholestyramine in hamsters fed a lithogenic diet.模拟血浆脂蛋白与胆汁脂质的关系:在喂食致石性饮食的仓鼠中,车前草和考来烯胺的不同影响。
Metabolism. 1993 Dec;42(12):1531-40. doi: 10.1016/0026-0495(93)90147-g.
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Competition in liver transport between chenodeoxycholic acid and ursodeoxycholic acid as a mechanism for ursodeoxycholic acid and its amidates' protection of liver damage induced by chenodeoxycholic acid.鹅去氧胆酸与熊去氧胆酸在肝脏转运中的竞争作为熊去氧胆酸及其酰胺类化合物保护鹅去氧胆酸诱导的肝损伤的机制。
Dig Liver Dis. 2000 May;32(4):318-28. doi: 10.1016/s1590-8658(00)80025-0.