Formation of Lithocholic Acid from Chenodeoxycholic Acid in the Rat. Bile Acids and Steroids 103.
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Protective effects of ursodeoxycholic acid on chenodeoxycholic acid-induced liver injury in hamsters
To investigate the effects of ursodeoxycholic acid (UDCA) on chenodeoxycholic acid (CDCA)-induced liver injury in hamsters, and to elucidate a correlation between liver injury and bile acid profiles in the liver.Liver injury was induced in hamsters by administration of 0.5% (w/w) CDCA in their feed for 7 d. UDCA (50 mg/kg and 150 mg/kg) was administered for the last 3 d of the experiment.At the end of the experiment, serum alanine aminotransferase (ALT) increased more than 10 times and the presence of liver injury was confirmed histologically. Marked increase in bile acids was observed in the liver. The amount of total bile acids increased approximately three-fold and was accompanied by the increase in hydrophobic bile acids, CDCA and lithocholic acid (LCA). UDCA (50 mg/kg and 150 mg/kg) improved liver histology, with a significant decrease (679.3 +/- 77.5 U/L vs 333.6 +/- 50.4 U/L and 254.3 +/- 35.5 U/L, respectively, P < 0.01) in serum ALT level. UDCA decreased the concentrations of the hydrophobic bile acids, and as a result, a decrease in the total bile acid level in the liver was achieved.The results show that UDCA improves oral CDCA-induced liver damage in hamsters. The protective effects of UDCA appear to result from a decrease in the concentration of hydrophobic bile acids, CDCA and LCA, which accumulate and show the cytotoxicity in the liver.
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Abstract Dietary lithocholic acid has been shown to induce a biliary proliferation or the ductular cell reaction in the chicken (Hunt et al., 1963), rabbit, guinea pig, rat, mouse (Hunt et al., 1964) and monkey (Hunt, 1965). This bile acid also elevates plasma lipids in the chicken (Leveille et al., 1963) and rabbit (Hunt et al., 1964). Holsti (1962) has reported that dietary chenodeoxycholic acid induces a hepatic biliary proliferation in the rabbit analogous to that seen with dietary lithocholic acid. It was therefore of interest to study the effects of chenodeoxycholic acid in the chicken since this species, like the rabbit, is extremely sensitive to dietary lithocholic acid; also, chenodeoxycholic acid has been reported to be a normal constituent of bile in the chicken (Anderson and Haslewood, 1957). Male Hy-Line White Leghorn chicks were fed a stock diet for one week and then received the basal diet previously described (Leveille…
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The purpose of this study was to determine whether in man unusual types of concentrations or bile acids were present in colonic polyps, colon carcinomas, or the adjacent, apparently normal tissue. Methods for the determination of soluble and tissue-bound bile acids were validated. Of 14 polyps analyzed, eight contained detectable levels of bile acid, predominantly chenodeoxycholic acid; no lithocholic acid was observed in either the tissue-bound or soluble bile acid fractions. Bile acids were found in four of nine samples of colon carcinoma; in one tumor, tissue-bound lithocholic acid was present. Bile acids were similarly found in seven of 10 samples of normal bowel taken adjacent to the carcinoma. In the soluble bile acid fraction, cholic acid was more abundant than chenodeoxycholic acid. There was no correlation between tissue histology and bile acid composition or concentration. Under the conditions used, this study did not disclose a relationship between tissue bile acids and colorectal histology.
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Chenodeoxycholic acid (CDCA) was fed to pregnant rats at the 0.25% level in the diet from Day 11 of gestation to delivery in order to evaluate the effects on (1) maternal tissue bile acid composition, (2) neonatal tissue bile acid composition and cholesterol-7α-hydroxylase activity, and (3) maternal, neonatal, and postnatal liver morphology. Feeding CDCA increased maternal lithocholic acid while significantly decreasing deoxycholic acid, cholic acid, and total bile acids. Feeding CDCA resulted in a significantly higher chenodeoxycholic acid pool in the neonates while neonatal plasma cholesterol and the 7α-hydroxylation of cholesterol was not significantly affected. Morphological examination of maternal, neonatal, and postnatal rat liver revealed no significant hepatotoxicity. This investigation has shown that (a) neonates of CDCA fed dams have a significantly greater pool of CDCA, suggesting maternal-to-fetal transfer of dihydroxy bile acids, (b) neonatal cholesterol-7α-hydroxylase activity and total tissue bile acid pools are not significantly altered by increased pool of CDCA, and (c) no hepatotoxic effects on maternal, neonatal, and postnatal livers were evident with gestational feeding of CDCA at the 0.25% level in the rat.
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Bile acids may promote experimental colonic cancer. Many studies correlate fecal bile acids and colorectal carcinomas. Little is known on bile acids in the colonic mucosa and their relation to luminal bile acids. We, therefore, studied bile acids in colonic wall and contents of normal female Wistar rats and after 14 days' administration of chenodeoxycholic acid or ursodeoxycholic acid (90 mg/kg daily), two bile acids used in medicamentous cholelitholysis. Both regimens increase total bile acids in colonic contents, ursodeoxycholic acid produces a higher rise in toxic lithocholic acid. In the colonic wall, only ursodeoxycholic acid causes an increase of most nonsulfated bile acids including lithocholic acid. Bile acid patterns do not correlate in colonic wall and contents. We conclude that increased colonic wall bile acids after ursodeoxycholic acid administration warrant control in man. In future colorectal carcinoma studies, not only fecal, but also mucosal bile acid concentrations should be correlated to carcinogenesis.
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