Effect of ursodeoxycholic acid administration on bile acid composition in hamster bile

Matejka, M.; Vescina, Cristina; Carducci, C. N.; ́n, A. Alayo; Dios, Aurora Escoto de; Scarlatto, E.; Mamianetti, A

doi:10.1016/1043-6618(90)90727-u

Cited by 8 publications

(1 citation statement)

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“…The transformation of UDCA into CDCA by hepaticbacterial interaction has been ob-served previously (44,45). Recent experiments in hamsters that were fed UDCA showed that the amount of UDCA in bile at the time the hamsters were killed is dose dependent and usually does not exceed 15% of total biliary bile acids, even when UDCA was fed at a dose of 2% (46). Presumably, in the Sasco hamster the epimerization of the 7p-hydroxyl group to the 7a-configuration occurred readily during long-term administration of UDCA or UDC-tau, reducing the hydrophilic character of the biliary bile acid mixture.…”

Section: Discussionmentioning

confidence: 99%

Bile Acid Sulfonates Alter Cholesterol Gallstone Incidence in Hamsters

et al. 1993

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The prevention of cholesterol gallstone formation by three bile acid analogs, sodium 3 alpha,7 alpha-dihydroxy-5 beta-cholane-24- sulfonate, sodium 3 alpha,7 beta-dihydroxy-5 beta-cholane-24-sulfonate and sodium 3 alpha,6 alpha-dihydroxy-5 beta-cholane-24-sulfonate, was examined in a hamster model of cholesterol cholelithiasis. Sodium taurochenodeoxycholate, sodium tauroursodeoxycholate and sodium taurohyodeoxycholate were studied simultaneously for comparison. Gallstones and cholesterol crystals were induced in 14 of 15 hamsters fed a bile acid-free, semipurified lithogenic diet containing 0.3% cholesterol and 4% butterfat for 6 wk. The addition of 0.1% sodium taurochenodeoxycholate and sodium tauroursodeoxycholate to the lithogenic diet had little effect on the formation of gallstones or biliary cholesterol crystals. In contrast, sodium 3 alpha,7 alpha-hydroxy-5 beta-cholane-24- sulfonate and sodium 3 alpha,7 beta-dihydroxy-5 beta-cholane-24-sulfonate, when fed at the same dose, prevented cholesterol gallstone formation significantly. Sodium taurohyodeoxycholate and sodium 3 alpha,6 alpha-dihydroxy-5 beta-cholane- 24-sulfonate inhibited cholesterol gallstone formation effectively. The cholesterol saturation index of bile was greater than 1.00 in all groups, with the exception of the group fed sodium 3 alpha,7 alpha-dihydroxy-5 beta-cholane-24-sulfonate. Liver and serum cholesterol levels tended to be lower in most of the groups that were fed bile acids. This effect was most pronounced in the animals receiving sodium taurohyodeoxycholate. At the end of the experiment, the administered sulfonate analogs were detected in gallbladder bile.(ABSTRACT TRUNCATED AT 250 WORDS)

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Section: Discussionmentioning

confidence: 99%

Bile Acid Sulfonates Alter Cholesterol Gallstone Incidence in Hamsters

et al. 1993

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Regulation of fecal bile acid excretion in male golden Syrian hamsters fed a cereal-based diet with and without added cholesterol

Turley

Spady

1997

Hepatology

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particular pharmacological agent or dietary treatment has The objective of these studies was to investigate the any effect on bile acid metabolism can be resolved by the comparative physiology and regulation of bile acid memeasurement of a number of related parameters. While the tabolism in the male Golden Syrian hamster by measurdetermination of bile acid pool size and composition provides ing the rate of fecal bile acid excretion and bile acid pool useful information, it is preferable to obtain a measure of the size in animals fed a cereal-based diet either alone, or overall rate at which cholesterol is degraded to bile acids. with added cholesterol or cholestyramine. In groupThis is now most widely performed by determining the activhoused hamsters fed only the plain diet fecal bile acid ity of cholesterol 7a-hydroxylase, the first and rate-limiting excretion in animals at 6, 10, and 15 weeks of age averstep in the biosynthetic pathway, or the level of messenger aged 11.0, 8.0, and 6.9 mmol/d per 100 g body weight (bw), RNA for this enzyme in the liver. [7][8][9][10][11] However, this approach respectively. Pool size, measured by subtracting from the total amount of bile acid washed out over 12 hours can be difficult because the basal level of activity of this enof biliary diversion the amount of bile acid excreted in zyme is very low in some species, and shows significant diurthe stools over the same period, equalled 17.8 mmol/100 nal variation in others.12,13 Furthermore, such measurements g bw in 15-week-old hamsters fed the plain diet. Hence, give only relative values and cannot be used to calculate the under basal conditions, these animals turned over about true amount of bile acid that is synthesized. The alternative 38% of their bile acid pool daily. In hamsters fed a diet approach is to determine the rate of fecal bile acid excretion, with 3% cholestyramine for 18 days, fecal bile acid excre-which under steady-state conditions provides a measure of tion averaged 20.6 mmol/d per 100 g bw, and the pool size the absolute rate of bile acid synthesis. contracted to 5.8 mmol/100 g bw. In matching animals fedAlthough there is an extensive literature on the comparaa diet containing 0.12% cholesterol for 30 days, hepatic tive physiology of several aspects of cholesterol and lipoprocholesterol levels increased from 1.9 { 0.1 to 12.6 { 0.7 tein metabolism in a number of different animal models, mg/g, fecal bile acid excretion increased marginally from there are few quantitative data relating to the basal rates of 5.8 to 8.0 mmol/day per 100 g bw, while pool size was bile acid synthesis in these particular species.14 Among these unchanged (16.6 mmol/100 g bw). When the cholesterol is the male Golden Syrian hamster which has proved to be an content of the diet was raised to 1.0%, hepatic cholesterol attractive model for investigating the mechanisms of action of levels reached 66.5 { 2.6 mg/g, but bile acid excretion many different classes of hypolipidemic agents [15][16][17][18][19][20][21] and also remained at 8 m...

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