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PubMed1969

Comparative studies of bile salts. Bile salts of the lamprey Petromyzon marinus L.

1. Bile salts of Petromyzon marinus L. ammocoetes appeared to consist solely or chiefly of a crystalline substance, whose chromatographic and i.r.-spectral characteristics suggested that it was a monosulphate ester of a bile alcohol having the 3alpha,7alpha,12alpha-trihydroxy pattern of substitution in a 5alpha-steroid nucleus. 2. This substance on cleavage with dioxan-trichloroacetic acid gave petromyzonol, n.m.r. and mass-spectral examination of which suggested the structure 5alpha-cholane-3alpha,7alpha,12alpha,24-tetrol. 3. 3alpha,7alpha,12alpha-Trihydroxy-5alpha-cholanoic acid (allocholic acid) from the lizards Anolis lineatopus lineatopus Gray and Cyclura carinata Harlan (family Iguanidae) was esterified with propan-1-ol and reduced by lithium aluminium hydride to 5alpha-cholane-3alpha,7alpha,12alpha,24-tetrol, identical with petromyzonol. 4. Chromic acid oxidation of petromyzonol sulphate from lamprey bile, followed by acid hydrolysis, gave 24-hydroxy-5alpha-cholane-3,7,12-trione; hence the sulphate ester group is at C-24. 5. Petromyzonol sulphate is both primitive and unique: a study of its biogenesis might improve our understanding of evolution at the molecular level.

Aluminum↗
PubMed1974

A more detailed study of bile salt evolution, including techniques for small-scale identification and their application to amphibian biles.

1. Methods have been developed for the isolation and identification of small amounts of bile salts and of bile acids and alcohols obtained by solvolysis. These methods involve preparative and analytical t.l.c., purification on columns of protonated Al(2)O(3) and Sephadex LH-20 and also g.l.c.-mass spectroscopy of solvolysis products. 2. Application to 29 species of frogs and toads has confirmed the constancy of bile salt patterns in a single species, including colour phases in two instances, and has revealed great variations between different species in some genera (e.g. Rana, Ptychadena) and little difference between widely distributed species in others (e.g. Bufo). 3. Taxonomic deductions should be made with caution and with regard to the physiological significance of the biochemical character considered. The molecular differences found might be interpreted as indicating variations in the rate of evolution.

Amphibians↗
PubMed1978

Glucuronic acid conjugates of bilirubin-IXalpha in normal bile compared with post-obstructive bile. Transformation of the 1-O-acylglucuronide into 2-, 3-, and 4-O-acylglucuronides.

Structures have been determined for bilirubin-IXalpha conjugates in freshly collected bile of normal rats, dogs and man and in post-obstructive bile of man and rats. The originally secreted conjugate has been characterized as azopigment (I), i.e. a 1-O-acyl-beta-d-glucopyranuronic acid glycoside. Conversion of the acetylated methyl ester of azopigment (I) into methyl 2,3,4-tri-O-acetyl-1-bromo-1-deoxy-beta-d-glucopyranuronate (V) indicates the pyranose ring structure for the carbohydrate and a C-1 attachment for the bilirubin-IXalpha acyl group. Alternative procedures for deconjugation of azopigment (I) and its derivatives are also described. In post-obstructive bile, the 1-O-acylglucuronide is converted into 2-, 3- and 4-O-acylglucuronides via sequential intramolecular migrations of the bilirubin acyl group. The following approach was utilized. (1) The tetrapyrrole conjugates were cleaved to dipyrrolic aniline and ethyl anthranilate azopigments, and the azopigments were separated as the acids or methyl esters. (2) The isomeric methyl esters were characterized by mass spectral analysis of the acetates and silyl ethers. (3) The free glycosidic function was demonstrated by 1-oxime and 1-methoxime derivative formation. (4) The position of the dipyrrolic O-acyl group was determined for the methyl esters by protecting the free hydroxyl groups of the glucuronic acid moieties as the acetals formed with ethyl vinyl ether and by further conversion of the carbohydrates into partially methylated alditol acetates. These were analysed by using g.l.c.-mass spectrometry. The relevance of the present results with regard to previous reports on disaccharidic conjugates is discussed. Details of procedures for the formation of chemical derivatives for g.l.c. and mass spectrometry have been deposited as Supplementary Publication SUP 50081 (15 pages) at the British Library Lending Division, Boston Spa, West Yorkshire LS23 7BQ, U.K., from whom copies can be obtained on the terms indicated in Biochem. J. (1978), 169, 5.

Animals↗
PubMed1995

Enhancement of Mdr2-mediated phosphatidylcholine translocation by the bile salt taurocholate. Implications for hepatic bile formation.

Expression of the Mdr2-protein in secretory vesicules (SVs) from the yeast mutant sec6-4 causes a time- and temperature-dependent enhancement of phosphatidylcholine (PC) translocation from the outer to the inner leaflet of the SV lipid bilayer. We show that this activity is independent of changes either in the membrane potential or the pH gradient (inside positive) generated in these SVs by the yeast proton-translocating PMA1 ATPase. However, loading of the SVs with the primary bile salt taurocholate results in an apparent enhancement of Mdr2-mediated PC translocation activity. Reducing the intravesicular taurocholate (TC) concentration by dissipating the electrochemical potential across the SV membranes eliminates the enhancing effect of TC. Three lines of evidence suggest that the enhanced Mdr2-mediated PC translocation activity is not caused by a regulatory effect of TC on Mdr2 but rather reflected the formation of TC/PC aggregates or micelles in the lumen of SVs. First, significantly higher detergent concentrations are required to reveal the fluorescence of (7-nitro-2-1,3-benzoxadiazol-4-yl)amino-PC molecules translocated in Mdr2-SV under conditions of TC stimulation than under control conditions; second, the nonmicelle-forming bile salt taurodehydrocholate does not cause enhancement of PC translocation in Mdr2-SVs; third, enzyme marker studies indicate that TC behaves as a potent lipid solubilizer directly extracting PC molecules out of the bilayer without causing leakage. This results in the formation of intravesicular aggregates or mixed micelles, and provokes the apparent stimulation of Mdr2 activity. These data demonstrate a unique relationship between Mdr2, PC, and TC in the process of bile formation and secretion.

4-Chloro-7-nitrobenzofurazan↗
PubMed1999

Identification of a bile acid-responsive element in the human ileal bile acid-binding protein gene. Involvement of the farnesoid X receptor/9-cis-retinoic acid receptor heterodimer.

Intestinal bile acid-binding protein (I-BABP) is a cytosolic protein that binds bile acids (BAs) with a high affinity. In the small intestine, its expression is restricted to the ileum where it is involved in the enterohepatic circulation of BAs. Using the human enterocyte-like Caco-2 cell line, we have recently shown that BAs increased I-BABP gene expression. To determine whether this regulation occurs in vivo, the effect of BA depletion or supplementation was studied in mice. A dramatic drop in I-BABP mRNA levels was observed in mice treated with the BA-binding resin cholestyramine, whereas an increase was found in animals fed with taurocholic acid. BAs are physiological ligands for the nuclear farnesoid X receptor (FXR). Both FXR and I-BABP are co-expressed along the small intestine and in Caco-2 cells. To determine the role of FXR in the regulation of I-BABP expression, the promoter of the human I-BABP gene was cloned. In Caco-2 cells, cotransfection of FXR and RXRalpha is required to obtain the full transactivation of the I-BABP promoter by BAs. Deletion and mutation analyses demonstrate that the FXR/RXRalpha heterodimer activates transcription through an inverted repeat bile acid responsive element located in position -160/-148 of the human I-BABP promoter. In conclusion, we show that FXR is a physiological BA sensor that is likely to play an essential role in BA homeostasis through the regulation of genes involved in their enterohepatic circulation.

Animals↗
PubMed1976

Comparison of the binding of various bile acids and bile salts in vitro by several types of fiber.

The binding in vitro of the sodium salts of cholic acid, chenodeoxycholic acid, deoxycholic acid, taurocholic acid, taurochenodeoxycholic acid, taurodeoxycholic acid, glycocholic acid, glycochenodeoxycholic acid, and glycodeoxycholic acid by alfalfa, bran, cellulose, lignin, and cholestyramine was measured. Cholestyramine bound an average of 81.3% of all the bile acids and salts tested whereas cellulose bound only negligible amounts (1.4%). Of the other substances tested, lignin bound 29.2%, alfalfa, 15.9% and bran, 9.0%. No distinct pattern of binding was discerned. It is therefore apparent that the validity of statements concerning the effect of fiber on bile salf metabolism rests upon the specificity of the composition of the fiber involved and the bile acids or salts tested.

Bile Acids and Salts↗
PubMed1976

A new bile acid conjugate, ciliatocholic acid, from bovine gall bladder bile.

This study was carried out to investigate the occurrence of ciliatocholic acid in bovine gall bladder bile. Ciliatocholic acid was synthesized according to the method described by Bergstrôm and Norman for the synthesis of taurocholic acid. Elemental analysis, melting point, and the infrared spectrum of this substance were determined. An isolation procedure for ciliatocholic acid was established by stepwise elution with an HCl-ethanol solvent system using a Dowex-1 anion exchange resin column chromatographic technique. Ciliatocholic acid amounting to 158 mug (as ciliatine) per 100 ml of gall bladder bile was found in the fraction eluted with 0.01 N HCl in 50% ethanol. This coumpound was purified by preparative thin-layer chromatography and confirmed to be ciliatocholic acid from the hydrolytic stability, phosphorus determination, and chromatographic behavior. Thus, bovine gall bladder bile contains a small amount of ciliatocholic acid.

Aminoethylphosphonic Acid↗
PubMed1989

Extracorporeal shock-wave lithotripsy of bile duct calculi. An interim report of the Dornier U.S. Bile Duct Lithotripsy Prospective Study.

A multi-institutional study to evaluate the efficacy, clinical application, and safety of extracorporeal shock-wave lithotripsy (ESWL) with the Dornier HM-3 or HM-4 lithotripter for bile duct calculi (BDC) was initiated in September, 1987. Symptomatic patients who entered into this prospective trial had BDC in the common bile duct and/or the intrahepatic, cystic or lobar ducts of the liver that were inaccessible or untreatable by papillotomy or percutaneous stone extraction. The study excluded gallbladder stones. Nasobiliary (54.4%) or transhepatic catheters (10.5%) and T-tube or cholecystostomy tubes (17.5%) or combinations (14.0%) permitted access for radiographic contrast to allow fluoroscopic monitoring of stone position and fragmentation. Exclusion criteria included pregnancy, failure to localize the stone, disturbances of coagulation, pacemakers, or vascular aneurysms or large bones that lie in the focal axis of the shock waves. Eleven institutions treated 42 patients (23 male, 19 female) with BDC; age range was 25 to 95 years (mean +/- SD, 73.5 +/- 13.8) and ASA risk category was 1 to 4 (mean, 2.3 +/- 0.8). Fourteen patients (33.3%) had a single BDC; 28 had 2 to 8 stones (mean, 2.7 +/- 1.8) ranging in size from 6 mm to 30 mm (mean, 18.5 +/- 6.4). The majority (66.7%) of patients were postcholecystectomy. The 42 patients received 57 ESWL treatments consisting of 600 to 2400 shocks per treatment (mean, 1924 +/- 289) at 12 to 22 kV (mean, 18.5 +/- 1.9) administered over 20 to 125 minutes (mean, 52.9 +/- 20.8). General anesthesia was used in 32% of the treatments; the majority were treated with epidural or regional block (42.1%), local infiltration (28.1%), or intravenous sedation (38.6%). Fifteen patients (35.7%) required two ESWL treatments. Stone fragmentation occurred in 94.6% of evaluable patients and in 90.4% of ESWL treatments, respectively; however, BDC fragments remained in 59.5% of patients 24 hours after treatment (diameter less than or to 3 mm, 12%; 4 to 9 mm, 16%; greater than or equal to 10 mm, 68%). Some patients (50%) required adjunctive procedures to achieve stone removal that included endoscopic extraction (n = 10; 47.6%), biliary lavage (n = 8; 38.1%), endoscopic bile duct prosthesis (n = 1; 4.8%), and operation (n = 2; 9.5%). ESWL treatment complications during hospitalization were observed in 15 patients (35.7%) and were present in four (9.5%) at discharge. Complications included macrohematuria (5%), biliary pain (15%), biliary sepsis (5%), hemobilia (10%), ileus (2.5%), and adverse pulmonary changes (7.5%). One patient developed pancreatitis before ESWL at ERCP that resolved prior to discharge.(ABSTRACT TRUNCATED AT 400 WORDS)

Adult↗
PubMed1984

Urinary bile acid and bile alcohol excretion does not reflect the genetic polymorphism of debrisoquine hydroxylation.

Excretion of the major urinary bile alcohol 27-nor-5 beta-cholestane-3 alpha, 7 alpha, 12 alpha, 24,25- pentol , and of cholic, chenodeoxycholic, deoxycholic and lithocholic acid was measured in 24 h urine collections of 10 extensive and seven poor metabolizers of debrisoquine. There was no significant difference of the excretion of these cholesterol metabolites between the two groups, indicating that cholesterol hydroxylation to bile alcohols and bile acids is probably not controlled by the same genes responsible for the 'debrisoquine-type' hydroxylation polymorphism.

Adult↗
PubMed2001

Bile salt hydrolase activity and resistance to toxicity of conjugated bile salts are unrelated properties in lactobacilli.

Bacteria of numerous species isolated from the human gastrointestinal tract express bile salt hydrolase (BSH) activity. How this activity contributes to functions of the microorganisms in the gastrointestinal tract is not known. We tested the hypothesis that a BSH protects the cells that produce it from the toxicity of conjugated bile salts. Forty-nine strains of numerous Lactobacillus spp. were assayed to determine their capacities to express BSH activities (taurodeoxycholic acid [TDCA] hydrolase and taurocholic acid [TCA] hydrolase activities) and their capacities to resist the toxicity of a conjugated bile acid (TDCA). Thirty of these strains had been isolated from the human intestine, 15 had been recovered from dairy products, and 4 had originated from other sources. Twenty-six of the strains expressed both TDCA hydrolase and TCA hydrolase activities. One strain that expressed TDCA hydrolase activity did not express TCA hydrolase activity. Conversely, in one strain for which the assay for TDCA hydrolase activity gave a negative result there was evidence of TCA hydrolase activity. Twenty-five of the strains were found to resist the toxicity of TDCA. Fourteen of these strains were of human origin, nine were from dairy products, and two were from other sources. Of the 26 strains expressing both TDCA hydrolase and TCA hydrolase activities, 15 were resistant to TDCA toxicity, 6 were susceptible, and 5 gave inconclusive results. Of the 17 strains that gave negative results for either of the enzymes, 7 were resistant to the toxicity, 9 were susceptible, and 1 gave inconclusive results. These findings do not support the hypothesis tested. They suggest, however, that BSH activity is important at some level for lactobacillus colonization of the human intestine.

Amidohydrolases↗
PubMed2003

Bile acid regulation of hepatic physiology: IV. Bile acids and death receptors.

Toxic bile acids facilitate Fas and tumor necrosis factor-associated apoptosis-inducing ligand (TRAIL) death-receptor oligomerization and activation. Bile acid modulation of death-receptor signaling is multifactorial and includes trafficking of Fas to the cell surface, enhancing TRAIL-R2/DR5 expression, and suppression of function of cFLIP, an antiapoptotic protein modulating death-receptor function. Because bile acid-associated death receptor-mediated apoptosis is a common mechanism for cholestatic hepatocyte injury, inhibition of death receptors and their cascades may prove useful in attenuating liver injury during cholestasis.

Animals↗
PubMed2006

Administration of r-VEGF-A prevents hepatic artery ligation-induced bile duct damage in bile duct ligated rats.

The hepatic artery, through the peribiliary plexus, nourishes the intrahepatic biliary tree. During obstructive cholestasis, the nutritional demands of intrahepatic bile ducts are increased as a consequence of enhanced proliferation; in fact, the peribiliary plexus (PBP) displays adaptive expansion. The effects of hepatic artery ligation (HAL) on cholangiocyte functions during cholestasis are unknown, although ischemic lesions of the biliary tree complicate the course of transplanted livers and are encountered in cholangiopathies. We evaluated the effects of HAL on cholangiocyte functions in experimental cholestasis induced by bile duct ligation (BDL). By using BDL and BDL + HAL rats or BDL + HAL rats treated with recombinant-vascular endothelial growth factor-A (r-VEGF-A) for 1 wk, we evaluated liver morphology, the degree of portal inflammation and periductular fibrosis, microcirculation, cholangiocyte apoptosis, proliferation, and secretion. Microcirculation was evaluated using a scanning electron microscopy vascular corrosion cast technique. HAL induced in BDL rats 1) the disappearance of the PBP, 2) increased apoptosis and impaired cholangiocyte proliferation and secretin-stimulated ductal secretion, and 3) decreased cholangiocyte VEGF secretion. The effects of HAL on the PBP and cholangiocyte functions were prevented by r-VEGF-A, which, by maintaining the integrity of the PBP and cholangiocyte proliferation, prevents damage of bile ducts following ischemic injury.

Animals↗
PubMed1984

Induction of rat hepatic and intestinal alkaline phosphatase activity produced by bile from bile duct-ligated animals.

Bile duct ligation caused a threefold elevation of not only hepatic but also intestinal alkaline phosphatase. The increase was transient in intestinal mucosa and peaked at 12 h. Hepatic phosphatase levels reached a plateau by 36 h. Intraperitoneal injection of bile from ligated animals into normal rats produced qualitatively similar results. Studies were performed to further characterize the induction of phosphatase activity in both tissues. The addition of bile from ligated animals to organ explants of liver and intestine produced a two- and threefold rise in activity, respectively. Therefore, neural and hormonal factors are not essential in producing this induction. The increased activity produced in vitro in both tissues was due to heat-stable and dialyzable factor(s) and was blocked by inhibitors of protein synthesis. In the intestine activity occurred over the entire brush border as demonstrated by electron microscopic histochemistry. In the liver, increased activity was noted over the entire plasma membrane and was not localized to the canalicular membrane. Tunicamycin treatment of liver and intestinal explants markedly suppressed the induced phosphatase activity. Simultaneous treatment with protease inhibitors restored some of the phosphatase activity. These findings suggest that glycosylation of the alkaline phosphatase might provide at least partial protection from proteolysis.

Alkaline Phosphatase↗
PubMed1985

Biosynthesis of bile acids in cerebrotendinous xanthomatosis. Relationship of bile acid pool sizes and synthesis rates to hydroxylations at C-12, C-25, and C-26.

To examine the defect in side-chain oxidation during the formation of bile acids in cerebrotendinous xanthomatosis, we measured in vitro hepatic microsomal hydroxylations at C-12 and C-25 and mitochondrial hydroxylation at C-26 and related them to the pool size and synthesis rates of cholic acid and chenodeoxycholic acid as determined by the isotope dilution technique. Hepatic microsomes and mitochondria were prepared from seven subjects with cerebrotendinous xanthomatosis and five controls. Primary bile acid synthesis was markedly reduced in cerebrotendinous xanthomatosis as follows: cholic acid, 133 +/- 30 vs. 260 +/- 60 mg/d in controls; and chenodeoxycholic acid, 22 +/- 10 vs. 150 +/- 30 mg/d in controls. As postulated for chenodeoxycholic acid synthesis, mitochondrial 26-hydroxylation of 5 beta-cholestane-3 alpha, 7 alpha-diol was present in all specimens and was 30-fold more active than the corresponding microsomal 25-hydroxylation. However, mean mitochondrial 26-hydroxylation of 5 beta-cholestane-3 alpha,7 alpha-diol was less active in cerebrotendinous xanthomatosis than in controls: 59 +/- 17 compared with 126 +/- 21 pmol/mg protein per min. As for cholic acid synthesis, microsomal 25-hydroxylation of 5 beta-cholestane-3 alpha,7 alpha,12 alpha-triol was substantially higher in cerebrotendinous xanthomatosis and control preparations (620 +/- 103 and 515 +/- 64 pmol/mg protein per min, respectively) than the corresponding control mitochondrial 26-hydroxylation of the same substrate (165 +/- 25 pmol/mg protein per min). Moreover in cerebrotendinous xanthomatosis, mitochondrial 5 beta-cholestane-3 alpha,7 alpha,12 alpha-triol-26-hydroxylase activity was one-seventh as great as in controls. Hepatic microsomal 12 alpha-hydroxylation, which may be rate-controlling for the cholic acid pathway, was three times more active in cerebrotendinous xanthomatosis than in controls: 1,600 vs. 500 pmol/mg protein per min. These results demonstrate severely depressed primary bile acid synthesis in cerebrotendinous xanthomatosis with a reduction in chenodeoxycholic acid formation and pool size disproportionately greater than that for cholic acid. The deficiency of chenodeoxycholic acid can be accounted for by hyperactive microsomal 12 alpha-hydroxylation that diverts precursors into the cholic acid pathway combined with decreased side-chain oxidation (mitochondrial 26-hydroxylation). However, side-chain oxidation in cholic acid biosynthesis may be initiated via microsomal 25-hydroxylation of 5beta-cholestane-3alpha,7alpha,12alpha-triol was substantially lower in control and cerebrotendinous xanthomatosis liver. Thus, separate mechanisms may exist for the cleavage of the cholesterol side chain in cholic acid and chenodeoxycholic acid biosynthesis.

Adult↗
PubMed1979

Common bile duct pressure and Oddi sphincter pressure in patients with common bile duct stones with and without juxta-ampullar diverticula of the duodenum.

Resting common bile duct pressure and Oddi sphincter pressure were measured in 16 patients with common bile duct stones, 8 having in addition a juxta-ampullar diverticulum. Pressure measurements were performed with an infused catheter introduced through an endoscope under direct vision. No significant differences in fasting common bile duct pressures were observed between the two groups. The Oddi sphincter had a phasic activity, and the peak pressure was similar in both groups.

Aged↗
PubMed2000

Diminished gene expression of ileal apical sodium bile acid transporter explains impaired absorption of bile acid in patients with hypertriglyceridemia.

Patients with type IV hyperlipoproteinemia, particularly those with familial hypertriglyceridemia (FHT), have impaired absorption of bile acid, a defect that may contribute to the hypertriglyceridemia ( J. Lipid Res. 1995. 36: 96;-107). To determine whether this absorption defect is a result of abnormal expression of the ileal apical sodium bile acid transporter (ASBT) gene, we biopsied the terminal ileum at colonoscopy in 28 subjects, 13 with hypertriglyceridemia and 15 control subjects. Of the 13 hypertriglyceridemic subjects, 10 had lipid profiles compatible with FHT (elevated very low density lipoprotein [VLDL] triglycerides with normal LDL cholesterol). ASBT mRNA levels were measured in these biopsies by RNase protection assay, using glyceraldehyde dehydrogenase mRNA as a reference. ASBT protein was quantitated by Western blotting with an antibody to the carboxy-terminal 20 amino acids of the protein. The mean +/- SEM ASBT mRNA level in the control group was 205.7 +/- 19.9 (arbitrary units) compared with 138. 7 +/- 19.1 for all 13 hypertriglyceridemics (P = 0.03) and 141.7 +/- 20.8 in the 10 FHT patients (P = 0.05). Commensurate with these mRNA levels, the mean ASBT protein level in the control group was 126.2 +/- 22.6 versus 58.8 +/- 13.8 in hypertriglyceridemics (P = 0.02) and 61.8 +/- 15.2 in the FHT patients (P = 0.05). We conclude that impaired absorption of bile acid in type IV hypertriglyceridemia results from diminished expression of the ASBT gene in terminal ileum.

Aged↗
PubMed1975

Specificity of oxidation of bile-salt hydroxyl groups by crude extracts of Pseudomonas testosteroni (ATCC 11996) used in determining bile salts.

Recent experimental evidence suggests that, presumably as a recent of mutation, crude extracts of Pseudomonas testosteroni (ATCC 11996) no contain amounts of 7alpha- and 12alpha-hydroxysteroid dehydrogenate activity that invalidate the results of bile-salt determinations. To confirm or deny this, we studied the specificity of hydroxysteroid dehydrogenase contained in crude extracts of currently available samples of this bacterium in the oxidation of bile-salt hydroxyl groups. The dehydrogenases in these extracts specifically oxidized 3alpha-hydroxyl groups of cholate, chenodeoxycholate, and deoxycholate anions. No significant amount of 12alpha- or 7alpha-hydroxysteriod dehydrogenase activity was detected. Currently available crude extracts of Pseudomonas testosteroni (ATCC 11996) are therefore suitable for bile-salt quantification.

Bile Acids and Salts↗
PubMed1976

Bile acids. XLIX. Allocholic acid, the major bile acid of Uromastix hardwickii.

Tauroallocholate is the major bile salt of the lizard, Uromastix hardwickii. Alkaline hydrolysis of bile from 25 gallbladders provided 1.21 g of acidic material, about 90% of which was allocholic acid. Analyses by gas-liquid chromatography, and mass spectrometry verified the presence of almost 10% of deoxycholic acid and smaller amounts of other 5alpha and 5beta-bile acids.

Animals↗