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Results for “Chenodeoxycholic Acid”

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PubMed1991

Efficacy and safety of ursodeoxycholic acid for dissolution of gallstone fragments: comparison with the combination of ursodeoxycholic acid and chenodeoxycholic acid.

A prospective, double-blind, randomized, single-center study was conducted to compare ursodeoxycholic acid alone with the combination of ursodeoxycholic acid and chenodeoxycholic acid for dissolution therapy of gallstone fragments after shock wave lithotripsy. Patients with single radiolucent gallstones up to 30 mm in diameter or up to three stones of similar total volume received either 750 mg ursodeoxycholic acid alone (group A, n = 138) or the combination of 500 mg ursodeoxycholic acid and 500 mg chenodeoxycholic acid (group B, n = 144) in a single bedtime dose. The bile acids were administered from 2 wk before electrohydraulic lithotripsy until 3 mo beyond complete disappearance of all fragments. Patient's characteristics, stones (group A, 82% single stones, maximum diameter 19 +/- 5 mm, mean +/- S.D.; group B, 82% single stones, 18 +/- 5 mm), lithotripsy treatment and follow-up period were not different between the two groups. Between the two groups, no statistically significant difference was found in the time required for complete clearance of the fragments (group A, median time = 15 mo; group B, median time = 13 mo; p = 0.7). At 12 mo after lithotripsy, the probability of complete clearance was 46% +/- 5% in group A and 49% +/- 5% in group B. Diarrhea occurred significantly more often in group B than in group A (p less than 0.001) and was the main reason for withdrawal of randomized medication. Severe adverse effects of the bile acids were not observed. It is concluded that monotherapy with ursodeoxycholic acid is as efficient as the combination of ursodeoxycholic acid and chenodeoxycholic acid for fragment dissolution after lithotripsy.(ABSTRACT TRUNCATED AT 250 WORDS)

Abdominal Pain↗

PubMed1983

Liver function and the diagnostic significance of conjugated cholic acid and chenodeoxycholic acid in serum of African patients with sickle cell disease.

Concentrations of two primary bile acids (cholic acid and chenodeoxycholic acid) were determined by radioimmunoassay in the serum of 15 African homozygous sickle cell patients, ages ranging from 4 to 22 years. The mean serum levels of the two primary bile acids studied were significantly elevated when compared with the normal mean values. About 67% of the patients had pathological elevation of both primary bile acids, thereby indicating some hepatobiliary damage. Serum conjugated cholic acid correlated significantly with serum chenodeoxycholic acid in the sickle cell disease (r = 0.91, p less than 0.001). The results suggest that radioimmunoassays of serum conjugated cholic acid and chenodeoxycholic acid in sickle cell disease may also serve as useful biochemical assays in predicting liver dysfunction in sickle cell disease.

Adolescent↗

PubMed1983

Comparative effects of ursodeoxycholic acid and chenodeoxycholic acid on bile acid kinetics and biliary lipid secretion in humans. Evidence for different modes of action on bile acid synthesis.

The effects of ursodeoxycholic acid on biliary lipid secretion and bile acid kinetics were determined in 12 men. For comparison, eight of the subjects were also treated with chenodeoxycholic acid using a crossover study design. The daily dose of each bile acid was 15 mg/kg body wt; each treatment period lasted for 5-6 wk. Kinetics of cholic acid and chenodeoxycholic acid, hepatic secretion rates of biliary lipids, and lipid composition of concentrated fasting duodenal bile were determined before and at the end of each treatment period. The synthesis rates of cholic acid and chenodeoxycholic acid were increased by approximately 80% and 40%, respectively, during treatment with ursodeoxycholic acid. The fractional catabolic rates of the two bile acids were increased by approximately 50%, whereas the pool sizes remained unchanged. Under similar conditions, administration of chenodeoxycholic acid reduced the pool size as well as the synthesis rate of cholic acid by approximately 70%. Ursodeoxycholic acid reduced the hepatic secretion of cholesterol to a higher extent (approximately 50%) than did chenodeoxycholic acid (approximately 30%). The secretion rates of bile acids and phospholipids remained essentially unchanged during the two treatment periods. Fasting duodenal (gallbladder) bile was unsaturated with cholesterol during both regimens. It is concluded that the two bile acids exert different effects on bile acid metabolism. The enhanced conversion of cholesterol to bile acids observed during ursodeoxycholic acid treatment may at least partly explain why ursodeoxycholic acid can reduce the biliary output of cholesterol without suppressing hepatic cholesterol synthesis.

Bile↗

PubMed1978

Choleretic properties of ursodeoxycholic acid and chenodeoxycholic acid in dogs.

Choleretic effects and properties of ursodeoxycholic and chenodeoxycholic acids given orally were investigated in comparison with dehydrocholic acid in conscious dogs with cholecystectomy. Ursodeoxycholic acid as well as chenodeoxycholic acid increased the bile flow and the concentrations of phospholipid, cholesterol and bile acids in the bile. After administration of either ursodeoxycholic acid or chenodeoxycholic acid, a great amount of each bile acid appeared in the bile. Ursodeoxycholic and chenodeoxycholic acids increased the outputs of phospholipid, cholesterol and bilirubin in the bile. On the other hand, dehydrocholic acid markedly decreased the concentrations and outputs of all the above materials in the bile, despite a considerable increase in the bile flow. After administration of dehydrocholic acid, 3alpha, 7alpha-dihydroxy-12-keto-cholanoic acid appeared in the bile instead of dehydrocholic acid. The results suggest that ursodeoxycholic and chenodeoxycholic acids are transported into the bile from the hepatic cells where they produce a choleresis due to the bile acid-dependent mechanism. Dehydrocholic acid is metabolized in the liver and the metabolites produced hydrocholeresis.

Animals↗

PubMed1981

Hepatic 3-hydroxy-3-methylglutaryl coenzyme A reductase activity and biliary lipid composition in man: relation to cholesterol gallstone disease and effects of cholic acid and chenodeoxycholic acid treatment.

The present work was undertaken in order to study whether or not there is a relation between hepatic HMG CoA reductase, hepatic cholesterol concentration, and biliary lipid composition. In 55 patients (10 with adenomyoma of the gallbladder wall, 45 with cholesterol gallstones) a liver biopsy together with gallbladder and hepatic bile were obtained at laparotomy under standardized conditions. Of the gallstone patients, twelve had been treated with cholic acid and ten with chenodeoxycholic acid in a dose of 15 mg.kg-1.d-1 for 6-8 weeks prior to operation. Hepatic bile was supersaturated with cholesterol both in cholesterol gallstone patients and in patients with gallbladder adenomyoma. Treatment with cholic acid reduced the cholesterol saturation of hepatic bile, although supersaturation persisted. During chenodeoxycholic acid treatment, hepatic bile became unsaturated in most of the patients. Hepatic cholesterol concentration was about 20% higher in patients with cholesterol gallstone disease than in gallstone-free controls. During treatment with cholic acid or chenodeoxycholic acid, hepatic cholesterol concentration was normalized. Microsomal HMG CoA reductase activity was similar in males and females with cholesterol gallstone disease and not different from that seen in the gallstone-free controls. Treatment with chenodeoxycholic acid resulted in a 40% reduction of HMG CoA reductase activity. Cholic acid had no effect. In gallstone-free controls and in bile acid-treated but not in untreated gallstone patients, saturation of hepatic bile correlated with HMG CoA reductase activity. It is concluded that treatment with chenodeoxycholic acid but not with cholic acid results in unsaturated hepatic bile. This unsaturation may in part be explained by a decreased hepatic HMG CoA reductase activity.

Adult↗

PubMed1993

Enzymatic formation of D-cysteinolic acid conjugated chenodeoxycholic acid in liver preparation from red seabream, Pagrosomus major.

The enzymatic formation of D-cysteinolic acid conjugated chenodeoxycholic acid in liver preparation from a marine teleost, wild and cultured red seabream, Pagrosomus major, was investigated. [24-14C]Chenodeoxycholic acid was incubated with taurine, glycine, or D-cysteinolic acid in the liver preparation in the presence of CoA, ATP, NAD+ and FAD. D-Cysteinolic acid could be conjugated efficiently with chenodeoxycholic acid to give chenodeoxycholyl-D-cysteinolic acid in both wild and cultured red seabream liver preparations, though the production rate was slower than that of the formation of chenodeoxycholyltaurine. Under the conditions employed, glycine was not utilized as the substrate for the conjugation at all. The formation of chenodeoxycholyl-D-cystenolic acid was decreased by the addition of various concentrations of taurine to the incubation mixture. These results suggest that bile acid-CoA: amino acid N-acyltransferase in red seabream is not able to distinguish taurine and D-cysteinolic acid as the substrate, probably because of their structural similarity. Consequently, D-cystenolic acid conjugated bile acids found in the bile of wild red seabream were thought to be synthesized in the liver of the fish utilizing the unusual amino acid, which originated from foods, prior to secretion into the bile.

Acyltransferases↗

PubMed1976

The medical treatment of cholesterol gallstones: experience with chenodeoxycholic acid.

Chenodeoxycholic acid has been administered to 50 patients with cholelithiasis and 8 with choledocholithiasis for a period of 15 months at doses varying between 2- and 15 mg/kg/day. Among the 50 patients with cholelithiasis, complete dissolution occurred in 16 and partial dissolution in 15 cases. Among the 8 patients with choledocholithiasis, complete dissolution occurred in 3 and partial dissolution in 2 cases. Lower doses were adopted in an attempt to determine the minimum effective daily dose required to produce gallstone dissolution and to lower the cholesterol saturation index (mean 1.52 +/- 0.73 before and 0.98 +/- 0.36 after treatment). Routine liver function tests were carried out before, during and after treatment; no significant alterations were produced by therapy. Studies of the antipyrine half-life, to estimate hepatic microsomial function were found to be normal (mean 13.61 +/- 2.62 before and 13.21 +/- 3.04 after treatment). In addition, histological investigations of the liver were described. This study confirms the efficacy of chenodeoxycholic acid in the treatment of cholesterol gallstones and gives an indication of the minimum effective dose (7.8 mg/kg/day). At the present doses, it has been shown that there are no substantial modifications in fundamental liver function.

Adult↗

PubMed1987

Simultaneous determination of pool sizes and fractional turnover rates, of deoxycholic acid, cholic acid and chenodeoxycholic acid in man by isotope dilution with 2H and 13C labels and serum sampling.

This paper describes a method for simultaneous determination of the kinetics of the three major bile acids in man using (2,2,4,4-2H4) deoxycholic acid, (24-13C) cholic acid and (24-13C) chenodeoxycholic acid. The gas chromatographic/mass spectrometric-selected ion monitoring technique used provided complete separation of deoxycholic acid, cholic acid and chenodeoxycholic acid, which permitted simultaneous measurement of isotope ratios for all three bile acids. Since measurement of all three pool sizes and fractional turnover rates in a single experiment requires different isotopic labels for deoxycholic acid and cholic acid, we investigated the in vivo stability and applicability of (2,2,4,4-2H4) deoxycholic acid as a stable isotope marker for isotope dilution studies in man. No consistent differences were observed between deoxycholic acid pool sizes and fractional turnover rates determined in serum samples after administration of (2,2,4,4-2H4) deoxycholic acid and (24-13C) deoxycholic acid. Simultaneous administration of (2,2,4,4-2H4) deoxycholic acid, (24-13C) cholic acid and (24-13C) chenodeoxycholic acid and isotope ratio measurements in serum permitted determination of pool sizes and fractional turnover rates of the three major bile acid and the 7 alpha-dehydroxylation fraction. Pool sizes, fractional turnover rates and synthesis rates (input rates) agreed well with data obtained previously with (24-13C) labels in independent studies.

Carbon Isotopes↗

PubMed1985

Inhibition of pepsin activity by ursodeoxycholic acids and chenodeoxycholic acids.

The bile salts of ursodeoxycholic acid, glycoursodeoxycholic acid, tauroursodeoxycholic acid, chenodeoxycholic acid, glycochenodeoxycholic acid, and taurochenodeoxycholic acid were each found to inhibit pepsin proteolytic activity in vitro at various concentrations against the refined substrate n-APDT. The sodium salt of ursodeoxycholic acid was the most potent pepsin inhibitor among those tested.

Animals↗

PubMed1996

Effects of ursodeoxycholic acid and chenodeoxycholic acid on major histocompatibility complex class I gene expression.

We investigated the effect of ursodeoxycholic acid on major histocompatibility complex class I gene expression in cultured human hepatoma cells. Ursodeoxycholic acid, which is now being used for the treatment of various autoimmune liver diseases, paradoxically increased the mRNA level of major histocompatibility complex class I. However, endogenous bile acids, for example, chenodeoxycholic acid, increased major histocompatibility complex class I mRNA expression more strongly compared with ursodeoxycholic acid. Concerning the interplay between ursodeoxycholic and chenodeoxycholic acids, these bile acids additively induced major histocompatibility complex class I mRNA expression. In contrast, when the total concentration of ursodeoxycholic and chenodeoxycholic acids was kept constant, the expression of major histocompatibility complex class I mRNA appeared to decrease in a dose-dependent manner with an increasing ratio of ursodeoxycholic acid. These findings indicate that the beneficial action of ursodeoxycholic acid may be related to this relative decrease in major histocompatibility complex class I gene expression.

Blotting, Northern↗

PubMed1979

7alpha-Dehydroxylation of cholic acid and chenodeoxycholic acid by Clostridium leptum.

The rate of 7alpha-dehydroxylation of primary bile acids was quantitatively measured radiochromatographically in anaerobically washed whole cell suspensions of Clostridium leptum. The pH optimum for the 7alpha-dehydroxylation of both cholic and chenodeoxycholic acid was 6.5-7.0. Substrate saturation curves were observed for the 7alpha-dehydroxylation of cholic and chenodeoxycholic acid. However, cholic acid whole cell K0.5 (0.37 micron) and V (0.20 mumol hr-1mg protein-1) values differed significantly from chenodeoxycholic acid whole cell K0.5 (0.18 micron) and V (0.50 mumol-1 hr-1 mg protein-1). 7alpha-Dehydroxylation activity was not detected using glycine and taurine-conjugated primary bile acids, ursodeoxycholic acid, cholic acid methyl ester, or hyocholic acid as substrates. Substrate competition experiments showed that cholic acid 7 alpha-dehydroxylation was reduced by increasing concentrations of chendeoxycholic acid; however, chenodeoxycholic acid 7alpha-dehydroxylation activity was unaffected by increasing concentrations of cholic acid. A 10-fold increase in cholic and 7alpha-dehydroxylation activity occurred during the transition from logarithmic to stationary phase growth whether cells were cultured in the presence or absence of sodium cholate. In the same culture, a similar increase in chenodeoxycholic acid 7alpha-dehydroxylation was detected only in cells cultured in the presence of sodium cholate. These results indicate the possible existence of two independent systems for 7alpha-dehydroxylation in C. Leptum.

Chenodeoxycholic Acid↗

PubMed1990

Biological properties of the 2-fluoro-beta-alanine conjugates of cholic acid and chenodeoxycholic acid in the isolated perfused rat liver.

The isolated perfused rat liver was used to examine the hepatic extraction, biliary secretion and effect on bile flow of the 2-fluoro-beta-alanine conjugates of cholic acid and chenodeoxycholic acid. The naturally occurring taurine and glycine conjugates of these bile acids were used for comparisons. The 2-fluoro-beta-alanine conjugates were extracted by the liver to a similar extent as the taurine and glycine conjugates. The biliary secretion rate and increase in bile flow were similar for all the cholic acid conjugates. On the other hand, the maximal biliary secretion rate of the 2-fluoro-beta-alanine conjugate of chenodeoxycholate was similar to that of the glycochenodeoxycholate, but 47% lower than that of taurochenodeoxycholate. In addition, the 2-fluoro-beta-alanine conjugate of chenodeoxycholate produced a decrease in bile flow that was comparable to that observed with the glycochenodeoxycholate (54% vs. 74%), but which was greater than that produced by the taurochenodeoxycholate (12%). In summary, these data demonstrate that the biological properties of the 2-fluoro-beta-alanine conjugates of cholic acid and chenodeoxycholic acid are not markedly different from those of the naturally occurring taurine and glycine conjugates. These data also suggest that the amino acid moiety can influence the biliary secretion and cholestatic properties of chenodeoxycholic acid conjugates.

Alanine↗

PubMed1991

Promotion of hepatocellular foci in female rats by chenodeoxycholic acid.

Chenodeoxycholic acid (CDC), a dihydroxylated primary bile acid, was evaluated for promotional activity in the liver of rats using a two-stage initiation-promotion model. CDC is a primary bile acid that can attain high concentrations in serum and liver during induced or naturally occurring hepatocellular disorders. Female Sprague-Dawley rats were injected once (i.p.) with diethylnitrosamine (DEN, 150 mg/kg) or sterile physiologic saline (SAL, 0.85% NaCl). Two weeks later, rats in each group were placed into one of two subgroups and fed either NIH-31 mash (Control) or NIH-31 mash containing 0.5% CDC for a 10 week period. At the end of the feeding period, blood and liver samples were collected for determination of bile acid profiles and quantitation of hepatocellular foci respectively. Serum samples were analyzed for concentrations of individual bile acids using a HPLC method that utilizes a post-column enzymatic reaction and fluorescence detection. Liver slices from the left hepatic lobe were stained for foci positive for placental glutathione S-transferase. In serum, significant increases occurred in concentrations of all forms of CDC and were accompanied by mild, insignificant increases in lithocholic acid. Decreased serum concentrations occurred in all forms of cholic and deoxycholic acids. Analysis of liver sections revealed that rats treated with DEN-CDC had significant increases in numbers and volume of foci compared to those treated with DEN-Control. For rats in groups DEN-CDC and DEN-Control, the numbers of foci per square centimeter were 32 and 12; per cubic centimeter, 2221 and 937; and the per cent volume of foci, 1.487 and 0.385 respectively. In this study, CDC was a promoter of hepatocellular foci. Because concentrations of CDC in liver and serum increase in a variety of hepatobiliary disorders, the possibility that increases in endogenous concentrations can enhance the formation of hepatocellular foci is being explored.

Animals↗

PubMed1986

Ursodeoxycholic acid, 7-ketolithocholic acid, and chenodeoxycholic acid are primary bile acids of the nutria (Myocastor coypus).

Because ursodeoxycholic and chenodeoxycholic acids are interconverted in humans via 7-ketolithocholic acid, bile acid metabolism was studied in the nutria (Myocastor coypus), the bile of which is known to contain these three bile acids. Relative concentrations of ursodeoxycholic (37% +/- 20%), 7-ketolithocholic (33% +/- 17%), and chenodeoxycholic (17% +/- 9%) acids in gallbladder bile were unchanged by 5-20 h of complete biliary diversion (n = 7). Injection of either [14C]cholesterol, [14C]ursodeoxycholic, [14C]7-ketolithocholic acid, or a mixture of [7 beta-3H]chenodeoxycholic acid and [14C]chenodeoxycholic acid into bile fistula nutria demonstrated that all three bile acids can be synthesized hepatically from cholesterol, that they are interconverted sparingly (2%-5%) by the liver, but that 7-ketolithocholic acid is an intermediate in the hepatic transformation of chenodeoxycholic acid to ursodeoxycholic acid. An animal that had been fed antibiotics showed an unusually elevated concentration of ursodeoxycholic acid in gallbladder and hepatic bile, suggesting that bacterial transformation of ursodeoxycholic acid in the intestine may be a source of some biliary chenodeoxycholic acid and 7-ketolithocholic acid.

Animals↗

PubMed1996

Formation of cholic acid and chenodeoxycholic acid from 7 alpha-hydroxycholesterol and 27-hydroxycholesterol by primary cultures of human hepatocytes.

It has been suggested that chenodeoxycholic acid is preferentially formed by the alternative or 'acidic' pathway of bile acid biosynthesis starting with 27-hydroxylation of cholesterol, while cholic acid is derived from 7 alpha-hydroxycholesterol which initiates the 'neutral' pathway. We have studied bile acid formation from each of these precursors using human hepatocytes cultured in a novel sandwich collagen configuration. Culture supernatants were analyzed using capillary gas chromatography and gas chromatography-mass spectrometry. 27-Hydroxycholesterol and 7 alpha-hydroxycholesterol were both found to be efficiently converted to cholic acid as well as chenodeoxycholic acid. Analysis of acidic intermediates after addition of 7 alpha-hydroxycholesterol to the cultures revealed a significant increase of side-chain oxygenated C24- and C27-steroids with a 3-oxo-7 alpha-hydroxy-delta 4-ring structure. These data indicate that (i) the 'neutral' pathway is connected to the 'acidic' pathway by side-chain oxidation of C27-steroids with a 3-oxo-7 alpha-hydroxy-delta 4-ring structure and that (ii) the relative formation of cholic acid and chenodeoxycholic acid is regulated by metabolic events distal to the initial hydroxylation at either position 7 or position 27 of the cholesterol molecule.

Adult↗

PubMed1993

Effect of ursodeoxycholic acid on the kinetics of cholic acid and chenodeoxycholic acid in patients with primary sclerosing cholangitis.

Treatment of patients with cholestatic liver diseases with ursodeoxycholic acid has been shown to have beneficial effects that may be related to a shift in the balance between hydrophilic and hydrophobic bile acids in favor of hydrophilic bile acids. During treatment of patients with primary sclerosing cholangitis with ursodeoxycholic acid, plasma concentrations of some endogenous bile acids decrease. To test whether the changes in plasma bile acids are due to decreases of their pool sizes or synthesis rates, we determined bile acid kinetics of cholic and chenodeoxycholic acid in six patients with primary sclerosing cholangitis, of whom four also had ulcerative colitis. All patients were studied before and 3 mo after the start of ursodeoxycholic acid treatment. Six healthy subjects served as controls. In patients with primary sclerosing cholangitis, pool sizes of cholic and chenodeoxycholic acid were considerably smaller than those in healthy controls; after ursodeoxycholic acid treatment they were unchanged. Fractional turnover and synthesis of cholic acid increased significantly after ursodeoxycholic acid administration. Fractional turnover of chenodeoxycholic acid also increased significantly, whereas synthesis of this bile acid was unchanged. Our data indicate that in patients with primary sclerosing cholangitis, pool sizes of bile acids are reduced. The decrease of levels of endogenous bile acids in plasma under ursodeoxycholic acid treatment despite unchanged bile acid pool sizes indicates redistribution of the bile acids into the enterohepatic circulation, probably because of improved hepatic clearance after ursodeoxycholic acid treatment.

Adult↗

PubMed1981

Serum cholic acid and chenodeoxycholic acid concentrations in neonatal hyperbilirubinemia.

Primary bile acid concentrations were measured in serum of 332 newborns with neonatal hyperbilirubinemia (serum total bilirubin level greater than 200 mumol/l) and compared with those of 95 nonhyperbilirubinemic neonates (serum total bilirubin level less than 200 mumol/l). The serum concentrations (mumol/l; mean +/- SEM) for cholic acid (8.78 +/- 0.44) and chenodeoxycholic acid (10.5 +/- 0.68) were significantly higher (p less than 0.001) in the hyperbilirubinemic group than in the controls (7.16 +/- 0.48 and 6.67 +/- 0.48, respectively). 80 (24%) of the hyperbilirubinemic newborns had true cholestasis (serum levels of cholic and/or chenodeoxycholic acid higher than mean +/- 2 SD in the reference group). The ratio of cholic to chenodeoxycholic acid was significantly higher (p less than 0.05) in the cholestatic group than in the hyperbilirubinemic newborns without cholestasis. There was no significant differences in the serum concentrations of alkaline phosphatase or lactate dehydrogenase between the cholestatic and noncholestatic groups. In the hyperbilirubinemic newborns, the primary bile acids were indiscriminately raised. Only 8 infants from the 332 newborns had jaundice at the age of 1 month. Of these 8 infants only 2 had neonatal cholestatic hyperbilirubinemia. It thus appears that measurement of serum primary bile acid concentrations has only limited diagnostic value in assessing the severity or prognosis of neonatal hyperbilirubinemia.

Chenodeoxycholic Acid↗

PubMed1980

Studies directed toward synthesis of quassinoids VII. Conversion of chenodeoxycholic acid to a delta-lactone quassinoid analog and generation of A-ring diosphenol acetate derivatives of deoxycholic acid.

Chenodeoxycholic acid was converted to a new 5,14-epi-28,30-dinorquassinoid analog. Two isomeric A-ring diosphenol acetate derivatives of deoxycholic acid were synthesized. A 3-oxo-5 beta-steroid was transformed to a 4-acetoxy-3-oxo-delta 4-steroid by treatment with base and oxygen or to a 2-acetoxy-3-oxo-delta 2-steroid by reaction with cupric chloride in refluxing acetic acid followed by acetylation. Ketene extrusion is a characteristic mass spectral fragmentation of these diosphenol acetates.

Chemical Phenomena↗