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At least 19 recordsLinked to original sources
PubMed1979

Radioimmunoassay of conjugated cholic acid, chenodeoxycholic acid, and deoxycholic acid from human serum, with use of 125I-labeled ligands.

We describe a method for radioimmunoassay of conjugated cholic acid, chenodeoxycholic acid, and deoxycholic acid in serum. In the method, 125I-labeled bile acid conjugates are used as the tracers along with antibodies raised against individual bile acid-bovine serum albumin conjugates. Antibody-bound and free bile acids were separated by polyethylene glycol precipitation (final concentration, 125 g/L). Before radioimmunoassay, 0.1-mL serum samples were precipitated with nine volumes of ethanol, and portions from the supernate were used in the assays. The lowest measurable amounts of the bile acids, expressed as pmol/tube, were: cholic acid conjugates, 2; chenodeoxycholic acid conjugates, 0.5; and deoxycholic acid conjugates. 2. Analytical recovery of bile acids added to bile acid-free serum ranged from 85 to 110%; intra-assay and inter-assay CVs ranged from 3.2 to 5.3% and from 5.3 to 12.2%, respectively. Concentrations (mean +/- SD) of the bile acid conjugates in serum from apparently healthy women and men (in mumol/L) were: cholic acid conjugates, 0.43 +/- 0.17 (n = 126); chenodeoxycholic acid conjugates, 0.47 +/- 0.23 (n = 111); and deoxycholic acid conjugates, 0.33 +/- 0.11 (n = 96). The values for primary bile acids were greatly increased in patients with various hepatobiliary diseases.

Chenodeoxycholic Acid↗
PubMed1978

Pool size, synthesis, and turnover of sulfated and nonsulfated cholic acid and chenodeoxycholic acid in patients with cirrhosis of the liver.

In 5 patients with cirrhosis of the liver sulfated and nonsulfated [14C]cholic acid and [14C]chenodeoxycholic acid were administered intravenously and the specific activity curves were determined. Specific activities declined exponentially and pool sizes, synthesis rates, and turnover rates of bile acids were calculated on the basis of a one-pool system. The biological half-life of cholic acid was 4.3 +/- 1.6 days (mean +/- SEM) and of chenodeoxycholic acid was 2.8 +/- 1.2 days. The half-life of cholic acid sulfate was 0.7 +/- 0.5 day and of chenodeoxycholic acid sulfate was 0.8 +/- 0.5 day. The pool size of cholic acid was 513 +/- 103 mg, of chenodeoxycholic acid, 477 +/- 77 mg, of cholic acid sulfate, 4.7 +/- 1.0 mg, and of chenodeoxycholic acid sulfate, 38.7 +/- 4.0 mg. The daily synthesis of cholic acid was 90 +/- 14 mg, of chenodeoxycholic acid, 118 +/- 6 mg, of cholic acid sulfate, 7.2 +/- 2.1 mg, and of chenodeoxycholic acid sulfate was 32.6 +/- 3.2 mg. The data indicate that sulfate esters of bile acids are significantly more rapidly excreted than are unsulfated bile acids. More than one-fourth of the chenodeoxycholic acid but less than one-tenth of the cholic acid formed was sulfated. The preferential sulfation of chenodeoxycholic acid is responsible for the more rapid turnover of chenodeoxycholic acid in comparison to cholic acid. Sulfation enhances the excretion and thereby prevents the accumulation of hepatotoxic concentrations of chenodeoxycholic acid in patients with cirrhosis of the liver.

Alkaline Phosphatase↗
PubMed1979

Enterohepatic circulation rates of cholic acid and chenodeoxycholic acid in man.

The rate of enterohepatic cycling of cholic acid and chenodeoxycholic acid was determined in five male subjects. Pool sizes were measured by isotope dilution technique after intraduodenal administration of 14C-labelled cholic and chenodeoxycholic acid. The hourly hepatic secretion rate of bile acids was determined by an intestinal perfusion technique. From these data the cycling frequency was calculated. Chenodeoxycholic acid circulated on an average 1.34 (range, 1.13--1.57) times faster than cholic acid, probably because chenodeoxycholic acid to a larger extent than cholic acid is absorbed from the proximal small intestine and thus partly bypasses the hepaticoileal circuit. This difference in cycling rate may have methodological as well as physiological implications.

Bile Acids and Salts↗
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↗
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↗
PubMed1977

Speed of change in biliary lipids and bile acids with chenodeoxycholic acid--is intermittent therapy feasible?

To see whehter intermittent chenodeoxycholic acid (CDCA) therapy is a potential alternative to continous treatment for gallstone dissolution, the speed of change in bile lipid composition was studied after starting and stopping CDCA therapy. In addition, the relationship between bile lipid composition and the proportions of the bile acids was examined. Bile-rich duodenal fluid was collected twice in the first week and then at approximately weekly intervals for four to six weeks, from six gallstone patients starting 13-15 mg CDCA.kg BW-1 day-1 and from another group of six patients whose treatment was stopped after gallstone dissolution. After starting treatment, the mean biliary cholesterol saturation index (based on criteria of Hegardt and Dam, 1971) decreased from 1-49 +/- SEM 0-17 to 0-92 +/- 0-13 at three weeks and 0-88 +/- 0-10 at four weeks, by which time bile lipid composition had become relatively constant. In patients whose treatment was stopped, bile reverted to its supersaturated state within one week, changing from an on-treatment mean saturation index of 0-74 +/- 0-10 to 1-15 +/- 0-15 in six to eight days after withdrawing CDCA. The proportion of conjugated CDCA in the biliary bile acids increased from 27-9 +/- 2-5% to 60-5 +/- 4-2% within four days and to 80-7 +/- 6-2% by four weeks after starting CDCA. When treatment was stopped, the proportion of CDCA reverted to pretreatment levels by two to three weeks. The saturation index was significantly related (P less than 0-001) to the percent of conjugated CDCA present, such that when the proportion of CDCA exceeded 70%, bile was almost invariably unsaturated. Since the mean time taken for bile to become unsaturated was not shorter than the time taken for bile to revert to its supersaturated state, it seems that intermittent treatment would not be adequate to maintain an unsaturated bile and is, therefore, unlikely to be as effective as continuous treatment in dissolving gallstones.

Adult↗
PubMed1977

Desaturation of bile and cholesterol gallstone dissolution with chenodeoxycholic acid.

The feeding of one of the major biliary bile acids, chenodeoxycholic acid, at a dose of 10 to 15 mg/kg per day causes the circulating bile acid pool to become greatly enriched in this bile acid. When chenodeoxycholic acid composes more than 70% of the biliary bile acids, the amount of cholesterol secreted in bile falls, and bile becomes unsaturated in cholesterol. If cholesterol gallstones are present and are exposed to this unsaturated bile, they will dissolve in 4 to 24 months in the majority of patients. Extensive clinical experience indicates that such medical therapy is safe, despite unequivocal toxicity of chenodeoxycholic acid in several nonhuman primates. When therapy is stopped, bile resaturates, and stones may recur. Since cholecystecomy is a rapid, safe, effective, and usually permanent treatment for all gallstones, the value of medical therapy remains uncertain at present, except for patients in whom surgery is inadvisable. Nonetheless, the demonstration that chenodeoxycholic acid ingestion will desaturate bile and induce gallstone dissolution would appear to be an important pharmacological advance.

Adult↗
PubMed1979

Conversion of 7-ketolithocholic acid to ursodeoxycholic acid by human intestinal anaerobic microorganisms: interchangeability of chenodeoxycholic acid and ursodeoxycholic acid.

Chenodeoxycholic acid, ursodeoxycholic acid and 7-ketolithocholic acid were incubated with human intestinal bacteria (source: 4 healthy males) at 37 degrees C for 72 hours in an anerobic condition. The bile acids of the products in culture medium were identified by three independent methods, thin layer chromatography, gas-liquid chromatography and GLC-mass spectrometry. Lithocholic acid, ursodeoxycholic acid and 7-ketolithocholic acid were observed in the culture of chenodeoxycholic acid. Lithocholic acid, chenodeoxycholic acid and 7-ketolithocholic acid were observed in the culture of ursodeoxycholic acid. Chenodeoxycholic acid and ursodeoxycholic acid were produced from 7-ketolithocholic acid. These data may suggest that chenodeoxycholic acid and ursodeoxycholic acid are interconvertible via 7-ketolithocholic acid by the mixed culture of human intestinal microorganisms under an anaerobic condition.

Anaerobiosis↗
PubMed1978

Isolation of 3beta,7alpha-dihydroxychol-5-enoic acid, an intermediate of chenodeoxycholic acid biogenesis, and 3alpha,7alpha-dihydroxychol-4-enoic acid from bladder bile of hens.

Two Lifschütz-positive C24-bile acids were isolated from bladder bile of hens. One of these was identified by isotope dilution experiments after conversion to a 3H-labeled compound, and also by GLC after methoxylation, as 3beta,7alpha-dihydroxychol-5-enoic acid, a key intermediate of chenodeoxycholic acid biogenesis. The other, to which the structure 3beta,7alpha-dihydroxychol-4-enoic acid had been assigned previously, was proved to be its 3alpha-epimer by several experiments. These findings favor the alternative pathway of chenodeoxycholic acid biogenesis proposed by Yamasaki and his associates.

Animals↗
PubMedDate not supplied

Methoxylation of 3beta,7alpha-dihydroxychol-5-en-24-oic acid, a key intermediate of chenodeoxycholic acid biogenesis, compared with that of its 7beta-epimer.

The conventional methods of gas liquid chromatography or mass spectrometry failed to be useful for the identification of the biliary 3beta,7alpha-dihydroxychol-5-en-24-oic acid, a key intermediate of chenodeoxycholic acid biogenesis. It has been preliminarily reported that this acid in human bile was successfully identified by gas chromatography-mass spectrometry, after the methoxylation of its allyl alcohol group. Physical as well as spectral properties of the methoxylation products derived from the acid were reported, compared with those from its 7beta-epimer.

Chemical Phenomena↗
PubMed1978

Polymorphism of chenodeoxycholic acid.

Polymorphism of chenodeoxycholic acid was studied by differential thermal analysis and X-ray diffraction. Four polymorphic forms (three crystalline and one amorphous) were characterized.

Chenodeoxycholic Acid↗