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PubMed1983

Effect of colonic perfusion with sulfated and nonsulfated bile acids on mucosal structure and function in the rat.

A single-pass perfusion system was used in conscious restrained rats to measure changes in water and electrolyte transport and in protein and deoxyribonucleic acid output after perfusing 5-15-mM solutions of sulfated or nonsulfated bile acids through the colon. Perfusion with 5 mM nonsulfated deoxycholic acid or chenodeoxycholic acid changed net water and sodium absorption to net secretion, provoked marked increases in protein and DNA output into the perfusion effluent, and caused microscopic mucosal damage. In contrast, perfusion with 5 and 15 mM sulfated deoxycholic acid or with 5 mM sulfated chenodeoxycholic acid had no effect on water and electrolyte transport and caused only modest changes in protein and DNA output. To see whether or not sulfated bile acid could prevent the effect of its nonsulfated parent compound on colonic structure and function, perfusion with a mixture of 5 mM nonsulfated and 10 mM sulfated deoxycholic acid was performed. This produced net secretion of water and sodium together with less marked increases of protein and deoxyribonucleic acid output and less pronounced microscopic mucosal damage than was seen after 5 mM nonsulfated deoxycholic acid alone. Finally, 5 mM nonsulfated cholic acid had no effect on water or sodium transport, but 5 mM sulfated cholic acid, with one alpha-hydroxyl group masked and two alpha-hydroxyl groups "exposed," reduced water transport. These results suggest that sulfation prevents the cathartic effect of alpha-dihydroxyl bile acids in the colon.

Animals↗

PubMed1975

Convenient non-chromatographic assays for the microbial deconjugation and 7alpha-OH bioconversion of taurocholate.

We described two convenient assay methods to estimate bile acid deconjugation and bile acid bioconversion at the 7alpha-OH position by individual microorganisms grown in media containing taurocholic acid. The methods are based on (i) a selective chemical assay for taurine conjugates previously described and (ii) the use of a cell-free preparation of 7alpha-hydroxysteroid dehydrogenase from Escherichia coli to directly quantify 7alpha-OH groups. These non-chromatographic approaches have been applied to the study of three model strains of intestinal organisms, E. coli, Bacteroides fragilis, and Clostridium perfringens, grown in standard media in the presence of purified tritiated taurocholate. Assay results were confirmed by thin-layer chromatography solvent systems designed to separate conjugated from unconjugated bile acid and unmodified cholic acid nucleus from 7alpha-OH bioconversion product(s) (primarily 3alpha, 12alpha dihydroxy, 7-keto-cholanoic acid). In addition, 7alpha-hydroxysteroid dehydrogenase activity was demonstrated in cell-free extracts of all three organisms. Of the three organisms, only C. perfringens was demonstrated to (i) deconjugate taurocholic acid, (ii) contain 3alpha-hydroxysteroid dehydrogenase activity, (iii) convert cholic acid into at least five labeled metabolites visible on thin-layer chromatography, and (iv) catalyze significant tritium exchange with water in the medium.

Bacteroides fragilis↗

PubMed1984

HPLC purification and preparation of antibodies to cholic acid-inducible polypeptides from Eubacterium sp. V.P.I. 12708.

The role of bile acid-inducible polypeptides in 7-dehydroxylation was investigated in Eubacterium sp. V.P.I. 12708. Cholic acid-inducible bile acid 7 alpha-, 7 beta-dehydroxylase, and delta 6 reductase activities co-eluted from a gel filtration high performance liquid chromatography (HPLC) column. Antibody (Ab) was prepared to these enzymatically active fractions, immunoadsorbed with uninduced cell extract coupled to Sepharose 4B, and used for immunoprecipitation of [35S]-methionine-labeled polypeptides. Ab immunoprecipitated polypeptides with molecular weights of 45,000, 27,000, and 23,500 from induced but not uninduced cell extracts. Immunoinhibition experiments showed that this Ab preparation inhibited (60%) bile acid 7 alpha-dehydroxylase activity in cell extracts. The 45,000 mol wt polypeptide was purified by (NH4)2SO4 fractionation, HPLC gel filtration, and HPLC-DEAE chromatography. Ab prepared to the 45,000 mol wt polypeptide immunoprecipitated only that polypeptide. This Ab, however, did not inhibit bile acid 7 alpha-dehydroxylase activity. Ab specific for the 27,000 mol wt polypeptide was prepared by partial purification and immunoadsorption with uninduced cell extracts. Immunochemical staining, following SDS-PAGE of crude cell extracts, shows a single immunoreactive protein band at 27,000 daltons. This Ab immunoprecipitated the 27,000 mol wt polypeptide as well as small amounts of the 45,000 and 23,000 mol wt polypeptides. Immunoinhibition studies showed that this Ab preparation inhibited (25%) 7 alpha-dehydroxylase activity. These data suggest that the 27,000 mol wt polypeptide is involved in enzyme catalysis. This does not, however, eliminate some role for the 45,000 and 23,500 mol wt polypeptides in bile acid metabolism in this organism.

Antibodies, Bacterial↗

PubMed2003

ATP-dependent transport of bile acid intermediates across rat liver peroxisomal membranes.

The bile acid intermediate 3alpha,7alpha,12alpha-trihydroxy-5beta-cholestanoic acid (THCA) is converted to cholic acid exclusively in peroxisomes by the oxidative cleavage of the side chain. To investigate the mechanism by which the biosynthetic intermediates of bile acids are transported into peroxisomes, we incubated THCA or its CoA ester (THC-CoA) with isolated intact rat liver peroxisomes and analyzed their oxidation products, cholic acid and 3alpha,7alpha,12alpha-trihydroxy-5beta-cholest-24-enoic acid. The oxidation of both THCA and THC-CoA was dependent on incubation time and peroxisomal proteins, and was stimulated by ATP. THC-CoA was efficiently oxidized to cholic acid and 3alpha,7alpha,12alpha-trihydroxy-5beta-cholest-24-enoic acid as compared with THCA, suggesting that THC-CoA is the preferred substrate for transport into peroxisomes. The oxidation of THC-CoA was significantly inhibited by sodium azide, verapamile, and N-ethylmaleimide. Furthermore, the stimulatory effect of ATP on the oxidation was not replaced by GTP or AMP. In addition, the ATP-dependent oxidation of THC-CoA was markedly inhibited by pretreatment of peroxisomes with proteinase K when peroxisomal matrix proteins were not degraded. These results suggest that an ATP-dependent transport system for THC-CoA exists on peroxisomal membranes.

Adenosine Triphosphatases↗

PubMedDate not supplied

Bile acid conjugation pattern in the isolated perfused rat liver during infusion of an amino acid formulation.

The influence of the taurine-containing amino acid mixture Trophamine on the pattern of bile acid conjugation was examined in the isolated perfused rat liver using cholic acid as the bile acid substrate. In all experiments, greater than 97% of the cholic acid appearing in bile was conjugated with taurine or glycine. The pattern of taurine and glycine bile acid conjugation, however, was dependent on the availability of taurine in the perfusate medium. Thus, in the absence of Trophamine infusion, the percentage of cholic acid conjugated with taurine (ie, taurocholate) declined throughout the course of the cholic acid infusion. Trophamine infusion increased the ratio of biliary taurocholate/glycocholate by 4.5-fold over that observed in the absence of the amino acid infusion. Increasing the amount of taurine in Trophamine by 2- or 5-fold resulted in a 1.8- and 4.3-fold increase, respectively, in the taurocholate/glycocholate ratio over that observed during the Trophamine infusion. Infusion of taurine alone, at an equimolar concentration of taurine as that in Trophamine, resulted in a similar taurocholate/glycocholate ratio as that observed during the Trophamine infusion. These data indicate that taurine availability, even in the presence of high concentrations of glycine and other amino acids in Trophamine, appears to be the most important factor in determining the pattern of bile acid conjugation in the isolated perfused rat liver.

Amino Acids↗

PubMed1975

The effect of chenodeoxycholic acid feeding on bile acid kinetics and fecal neutral steroid excretion in patients with hyperlipoproteinemia types II and IV.

The kinetics of 24-14C-cholic acid and 3H-chenodeoxycholic acid and the elimination of cholesterol as fecal neutral steroids were studied in 6 patients with Type II and 7 patients with Type IV lipoprotein pattern before and during the ingestion of 0.8 to 1.0 Gm. of chenodeoxycholic acid per day. During treatment, the pool size of chenodeoxycholic acid increased in all subjects (not studied in one Type IV patient). In Type II patients, this effect was associated with a decrease of the cholic acid pool size from 868 +/- 141 to 213 +/- 51 mg. and of the cholic acid synthesis from 204 +/- 36 to 54 +/- 20 mg. per day. In the patients with hyperlopoproteinemia Type IV, the cholic acid pool size diminished in 6 of the 7 subjects all of whom showed a decrease in the cholic acid synthesis on the average from 607 +/- 155 to 202 +/- 44 mg. per day. It is suggested that the feedback control of cholic acid synthesis is less sensitive in the Type IV than in the Type II patients. Chenodeoxycholic acid feeding did not influence the fecal excretion of cholesterol, coprostanol, and coprostanone in a consistent way.

Adult↗

PubMed1981

A new method for the measurement of bile acid turnover and pool size by a double label, single intubation technique.

A new method is described for measuring the cholic acid turnover and pool size by a single duodenal intubation technique. The method is based on determination in a single bile sample of the ratio of the specific activities of [14C]cholic acid and [3H]cholic acid administered intravenously with an interval of 24 hr. With this ratio the fractional turnover rate (k) of cholic acid can easily be calculated as well as the half-life and pool size. Studies in ten normal subjects indicate that the cholic acid half life and pool size, determined by this single intubation technique, correlate very well (r greater than or equal to 0.98) with the results obtained by Lindstedt's method. Unlike the other methods using a single intubation, this method allows a good estimate of the bile acid turnover as well as the bile acid pool size.

Adult↗

PubMed1985

Cholesterol esterase activity of human intestinal mucosa.

It has been suggested that cholesterol absorption in humans is dependent on bile acid pool composition and that expansion of the cholic acid pool size is followed by an increase of the absorption values. Similar observations were reported in rats, where the increase of cholesterol absorption, after trihydroxy bile acid feeding, seems to be due to the stimulatory effect of cholic acid on the intestinal cholesterol esterase. In the present study, therefore, we investigated some general properties of human intestinal cholesterol esterase, with particular emphasis to the effect of bile acids on this enzymatic activity. Twenty-nine segments of small intestine were taken during operations; the enzymatic activity was studied by using mucosal homogenate as a source of enzyme and oleic acid, cholesterol, and 14C-labeled cholesterol as substrates. The time-activity relationship was linear within the first two hours; optimal pH for esterification ranged between 5 and 6.2. There was little difference between the esterifying activity of the jejunal and ileal mucosa. Esterification of cholesterol was observed with all the investigated fatty acids but was maximal with oleic acid. Bile acids did not affect cholesterol esterase activity when present in the incubation mixture at 0.1 and 1.0 mM; the enzymatic activity, however, was significantly inhibited when bile acids were added at 20 mM. In conclusion, this study has shown that the human intestinal mucosa possesses a cholesterol esterase activity; at variance with the rat, however, the human enzyme does not seem to be stimulated by trihydroxy bile acids. Thus, the stimulatory effect of cholic acid on cholesterol absorption induced by the administration of this bile acid does not seem to be simply due to changes of cholesterol esterase activity of the small bowel mucosa.

Adult↗

PubMed1978

Influence of cholestyramine on synthesis of cholesterol and bile acids in germfree rats.

The present investigation describes the influence of partial, pharmacologic interruption of bile acid enterohepatic circulation on cholesterol and bile acid synthesis in germfree rats. Seven rats received a basal, semisynthetic diet and five rats received the basal diet supplemented with 5% cholestyramine. After 6 weeks, feces were collected in one 3- and one 4-day pool for analysis of bile acids and cholesterol. When the sampling period was concluded, the rats were killed and the liver microsomal fractions were isolated. The activities of HMG CoA reductase and 7alpha-hydroxylase were determined. The main fecal bile acids in the untreated rats were cholic acid and beta-muricholic acid. During cholestyramine treatment cholic acid increased from 4.4 +/- 0.7 to 39.5 +/- 5.6 mg/kg body weight/day and beta-muricholic acid from 4.5 +/- 0.6 to 7.7 +/- 0.9 mg/kg body weight/day. Chenodeoxycholic acid became a major bile acid averaging 10.4 +/- 1.6 mg/kg body weight/day. The total amount of bile acids increased about 6-7 times and the percentage of cholic acid increased from 49.4 +/- 2.0 to 68.6 +/- 1.1%. The 7alpha-hydroxylase activity increased 4-5 times. During cholestyramine treatment the fecal excretion of cholesterol was increased from 12.0 +/- 1.4 to 68.0 +/- 5.0 mg/kg body weight/day. The endogenous formation of cholesterol was increased 6 times and the HMG CoA reductase activity was increased about 20 times. In conclusion, germfree rats, like conventional rats, have the ability to increase the endogenous formation of bile acids and cholesterol during interruption of the enterohepatic circulation of bile acids, which is also reflected in a stimulation of the activities of the rate-determining enzymes.

Animals↗

PubMed1982

Kinetics of primary bile acids in patients with non-operated Crohn's disease.

The metabolism of cholic acid and chenodeoxycholic acid was studied in seventeen patients with non-operated Crohn's disease, eleven ileitis and six ileocolitis patients. The turnover of cholic acid was significantly increased in patients with ileitis (k = 2.01 +/- 1.13 days-1; P less than 0.001) and ileocolitis (k = 0.91 +/- 0.47 days-1; P less than 0.005) as compared to normals (k = 0.35 +/- 0.19 days-1). Although chenodeoxycholic acid was better preserved in the enterohepatic circulation than cholic acid its turnover was also significantly faster in ileitis (k = 0.81 +/- 0.56 days-1; P less than 0.005) and ileocolitis patients (k = 0.62 +/- 0.18 days-1; P less than 0.01) than in normals (k = 0.20 +/- 0.09 days-1). The fractional turnover of cholic acid was related to the length of ileal involvement (r = 0.761; P less than 0.001; n = 17). Patients with Crohn's ileitis tended to preserve normal fasting total bile acid pools by increased synthesis of primary bile acids and efficient absorption of deoxycholic acid and ursodeoxycholic acid by the normal colon. Patients with active ileocolitis had decreased total fasting pool sizes (2.62 +/- 1.83 mmol; P less than 0.001) as compared to normals (7.69 +/- 1.61 mmol). In these patients there was no increase in bile acid synthesis as compared to normals and secondary bile acids were absent from bile. It is concluded that the colon has an important role in maintaining the fasting pool size to a normal level in the presence of an interrupted enterohepatic circulation of bile acids due to ileal disease.

Adolescent↗

PubMed1992

Effects of aminotriazole treatment on biosyntheses of primary bile acids in vivo.

The influence of aminotriazole treatment on primary bile acid biosynthesis was studied in detail. After administration of aminotriazole to rats, bile was collected for 8 h. The content of chenodeoxycholic acid in the bile was increased to 144% of the control by aminotriazole treatment, but that of cholic acid was decreased to 48.4%. In another experiment, [4-14C]cholesterol was injected into rats immediately after aminotriazole treatment, and then bile was collected. The content of radioactive chenodeoxycholic acid in the bile was significantly increased to 130% of the control, but that of radioactive cholic acid was unchanged. In a similar experiment with [2-14C]mevalonate, the content of radioactive chenodeoxycholic acid in the bile was hardly changed by aminotriazole treatment, but that of radioactive cholic acid was greatly decreased to 41.2% of the control. Aminotriazole treatment did not affect the ratios of tauroconjugate to glycoconjugate of the two bile acids. Thus, aminotriazole treatment affects the syntheses of not only cholesterol (F. Hashimoto, C. Sugimoto and H. Hayashi, Chem. Pharm. Bull., 38, 2532 (1990); F. Hashimoto and H. Hayashi, Biochim. Biophys. Acta, 1086, 115 (1991)) but also primary bile acids in vivo. Namely, aminotriazole treatment activated biosynthesis of chenodeoxycholic acid from exogenous cholesterol, but did not affect that of cholic acid. Aminotriazole hardly affected the synthesis of chenodeoxycholic acid through endogenous cholesterol (from mevalonate), but inhibited that of cholic acid.

Amitrole↗

PubMed1975

Bile acids and colonic motility in the rabbit and the human.

Colonic motor activity was initiated by infusions of bile salts into the caecum or rectum of the anaesthetized rabbit. Primary bile acids were examined proximally and distally in the colon and elicited marked motor responses. Sinc dihydroxy bile acids are known to be potent inhibitors of electrolyte and water absorption in the colon, the secondary bile acid deoxycholic acid, the dihydroxyl compound most related to cholic acid which is the main bile acid in the rabbit, was examined distally and was also active, but to a lesser extent than cholic acid conjugates in this species. In man, a relationship was found between the faecal bile acid excretion and colonic motility: the introduction of bile acids directly into the human sigmoid colon and rectum also stimulated colonic motility. In man, the dihydroxy compound chenodeoxycholic acid was slightly more active than conjugates of cholic acid.

Animals↗

PubMed1984

Spectrofluorimetric determination of desoxycholic acid in the presence of cholic and chenodesoxycholic acids by use of Ce(IV) and concentrated sulphuric acid.

A method for the quantitative estimation of desoxycholic acid (200-700 micrograms/ml) in the presence of cholic and chenodesoxycholic acids is described. The method is based on the transformation of desoxycholic acid in fluorescent products (lambda ex = 350 nm, lambda em = 458 nm) by the action of concentrated sulphuric acid, this being enhanced by the presence of Ce(IV). The sample is mixed with a solution of Ce(IV) and concentrated sulphuric acid under standard conditions. Fluorescence is measured in relation to a reference containing the same components except Ce(IV). Cholic and chenodesoxycholic acids do not produce a reaction under adequate conditions. Synthetic samples of bile acids were tested for validation of the method.

Cerium↗

PubMed1980

Amniotic fluid bile acids in normal and pathologic pregnancy.

Radioimmunologic techniques were used to determine 2 primary bile acids (cholic and chenodeoxycholic acid) and 1 secondary bile acid (deoxycholic acid) from human amniotic fluid of healthy pregnant women and from patients with diabetes, toxemia, or intrahepatic cholestasis during pregnancy. In general, the mean bile acid concentrations in the amniotic fluid were very similar to those in the serum, although in paired samples from individual patients these 2 values did not correlate significantly. Very high levels of the 2 primary bile acids were measured from the amniotic fluid of patients with intrahepatic cholestasis. The mean values were about 70 times higher than those in the controls. Amniotic fluid cholic acid content was slightly elevated in diabetic and toxemic patients, too. Deoxycholic acid was consistently found in the amniotic fluid specimens, but there was no change in its concentration among the various groups. In this limited series of patients, no significant correlation was found between the bile acid concentrations in the amniotic fluid and signs of fetal distress at the time of amniocentesis, although the lowest maternal serum estriol and human placental lactogen values were associated with the highest amniotic fluid bile acid concentrations. The condition of the newborn infants did not correlate with amniotic fluid bile acid concentrations in any of the patient groups studied. It thus appears that high amniotic fluid bile acid content present a threat to the fetus, but further studies are needed to clarify this point.

Adult↗

PubMed1991

Analysis of duodenal bile acids by high performance liquid chromatography in infants with cholestasis.

Non-sulfated bile acid levels including cholic acid (CA), chenodeoxycholic acid (CDCA), deoxycholic acid (DCA), lithocholic acid (LCA), ursodeoxycholic acid (UDCA), five taurine conjugates, and five glycine conjugates in duodenal juice were measured in 50 Chinese infants with cholestasis to test their diagnostic value. All 17 with biliary atresia (BA) cases, 11 out of 26 neonatal hepatitis (NH) cases and one case with paucity of the interlobular bile duct were without detectable bile acids. In those NH patients with detectable bile acids, the major components were conjugated forms of CA and CDCA, which was similar to all 6 cases of the comparison group with other diseases. The minor bile acid components identified in them were glycine conjugated UDCA, free CDCA, free CA, and free and conjugated DCA. Only one patient with NH had taurine conjugated LCA. The mean total duodenal bile acid level in 15 patients with NH was significantly lower than that in the 6 patients of the comparison group. Most patients with NH had a CDCA/CA ratio of less than one, indicating that cholic acid is the predominant form in their bile. Glycine conjugated bile acids were the predominant bile acids present in 11 out of 15 patients with NH and 4 out of 6 of the comparison group patients. The results suggest that the detection of duodenal bile acids by a sensitive HPLC method is of limited value in making a differential diagnosis between BA and NH.(ABSTRACT TRUNCATED AT 250 WORDS)

Bile Acids and Salts↗

PubMed1987

Aspects of the effect of bile salts on Candida albicans.

Cholic acid, chenodeoxycholic acid, deoxycholic acid, glycocholic acid, glycodeoxycholic acid, hyodeoxycholic acid and lithocholic acid as their sodium salts, were fungistatic to the growth of Candida albicans. Of the compounds tested, cholic acid, deoxycholic acid and chenodeoxycholic acid were the most active. In combination with other antifungal agents only cholic acid exhibited synergism with amphotericin B, whilst the imidazole antifungal agents inhibited the action of the bile salts. The bile salt minimal inhibitory concentrations were close to the critical micelle concentrations. Even though the compounds are surface active they did not cause loss of intracellular K+ and were without effect on oxygen consumption. The bile salts, particularly cholic acid, produced morphological changes that gave rise to swollen cells.

Amphotericin B↗

PubMed1993

Differential feedback regulation of cholesterol 7 alpha-hydroxylase mRNA and transcriptional activity by rat bile acids in primary monolayer cultures of rat hepatocytes.

We have used primary monolayer cultures of rat hepatocytes to study the effects of physiological concentrations of various bile acids, commonly found in bile of normal rats, on the mechanism of regulation of cholesterol 7 alpha-hydroxylase and bile acid synthesis. Addition of taurocholic acid, the most predominant bile acid in rat bile, to the culture medium suppressed cholesterol 7 alpha-hydroxylase activity and mRNA time- and dose-dependently. The decrease in enzyme activity paralleled the changes in mRNA. Maximal suppression of cholesterol 7 alpha-hydroxylase mRNA (-91%) and enzyme activity (-89%) was observed after a 16 h incubation period with 50 microM taurocholic acid. The declines in mRNA and enzyme caused by taurocholic acid were tightly coupled and followed first-order kinetics with a half-life of 4 h. Transcriptional activity, as assessed with nuclear run-on assays, was decreased by 44% at 50 microM taurocholic acid. Mass production of bile acids (chenodeoxycholic acid and beta-muricholic acid) was inhibited to a similar extent as the cholesterol 7 alpha-hydroxylase when different concentrations of taurocholic acid were used, giving maximal inhibition (-81%) at 50 microM taurocholic acid. Glycocholic acid and unconjugated cholic acid were equally effective as taurocholic acid in suppressing cholesterol 7 alpha-hydroxylase mRNA. The more hydrophobic bile acids (chenodeoxycholic acid and deoxycholic acid) showed profound suppression of the cholesterol 7 alpha-hydroxylase mRNA by 85% and 75% respectively, whereas the other trihydroxy bile acids in rat bile, alpha- and beta-muricholic acid, were not or only marginally active. We conclude that rat bile acids, in particular the more hydrophobic ones, in concentrations commonly observed in portal blood, exert negative feedback control at the level of cholesterol 7 alpha-hydroxylase mRNA in cultured rat hepatocytes through a direct effect on the hepatocytes, and that down-regulation of transcription is only one of the mechanisms involved in this regulation.

Animals↗

PubMed1983

Radioimmunoassay of bile acids in tissue, bile, and urine.

Two commercially available (Abbott Labs.) radioimmunoassays for determination of conjugated cholic acid and sulfoglycolithocholic acid in serum have been modified for bile acid measurements in alcoholic tissue extracts, bile, and urine. The specificity of both radioimmunoassays has been determined with regard to 27 free and conjugated bile acids. After filtration, bile acids can be measured in urine and bile without prior extraction. Tissue is homogenized and the bile acids are extracted into methanol. Urinary excretion by 64 healthy humans was 2.09 (SD 1.09) mumol of conjugated cholic acid and 8.44 (SD 8.03) mumol of sulfated glycolithocholic acid per 24 h. In liver from 10 patients with various noncholestatic liver disease, the mean concentration of conjugated cholic acid was 32.4 (SD 15.9) nmol/g wet weight. In the liver of 27 male Wistar rats, the concentration of conjugated cholic acid was 41.3 (SD 11.7) nmol/g of tissue, of sulfoglycolithocholic acid 5.1 (SD 2.3) nmol/g of tissue.

Adult↗