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PubMed2002

[Cholic acid metabolism in human fecal cultures during diet supplementation with Lacto-bacillus rhamnosus GG].

BACKGROUND: Lactobacillus rhamnosus GG is used as probiotic and is thought to have protective properties in the human gastrointestinal tract and in other organs. Enrichment of the bile acid pool with secondary bile acids is common in some hepatic and gastrointestinal diseases and this is considered as a pathogenic element in the disease progression. The aim of this study was to evaluate the effect of probiotic feeding on fecal bile acid biotransformation, particularly on the production of secondary bile acids. METHODS: Six normal volunteers were administered 500 g/die of a yogurt preparation containing 4 x 10(9) C.F.U. of Lactobacillus rhamnosus GG for 30 days. The 7alpha-dehydroxylation activity was investigated following addition of cholic acid to the stool samples collected before and after the probiotic feeding. The production of deoxycholic acid and the decrease in cholic acid level were studied. RESULTS: The comparison of biotransformation rate of cholic acid to deoxycholic acid before and after probiotic feeding didn't reach a statistically significant difference, but a strong difference was seen in three of the six subjects, indicating a different behavior in different groups of healthy subjects. Furthermore, the three non responder subjects had a lower fecal 7alpha-dehydroxylation activity in the stool samples from the pre-treatment collection. CONCLUSIONS: These results indicate that subjects with a higher production of secondary bile acids in stools may represent a target group for a larger trial with oral probiotic administration.

English Abstract↗
PubMed1986

Effect of dietary calcium and cholic acid on the proliferative indices of murine colonic epithelium.

The effect of dietary calcium on the cholic acid-induced colon cell proliferative response was investigated with C57BL/6J mice. The control diets were formulated on the basis of the AIN-76 diet with the levels of calcium set at 0.1, 0.5 or 1.0% by weight and the ratio of Ca:P at approximately 1:1. Cholic acid was added at 0.1% and 0.25% by weight. The cytokinetic parameters of the colons were evaluated after 2 weeks of feeding by the metaphase arrest technique and by autoradiography. Mitotic activity was found to monotonically decrease with increasing calcium level from 0.1 to 1.0% for both the cholic acid and control groups, cholic acid-fed groups exhibiting significantly higher mitotic activity than the control groups. The effect of calcium (0.1 versus 1.0%) was evident throughout the 24-h period with both the control and cholic acid-supplemented diets. Autoradiographic analyses of the colons yielded similar results. Among the controls, the 0.1% Ca group exhibited significantly higher (P less than or equal to 0.05) crypt height, higher whole crypt labelling index and higher labelling indices at various positions along the crypt height than the 1.0% Ca group. Cholic acid-fed groups had higher values for crypt height, whole crypt labelling indices and the position of the uppermost labelled cells than the control groups. The level of calcium affected the bile acid-induced cell proliferation in the colonic epithelium; the groups fed 0.1% Ca + cholic acid had a markedly higher whole crypt labelling index, a higher position of the uppermost labelled cells and higher labelling indices at various cell positions along the crypt column compared with the 1.0% Ca + cholic acid group. The present study thus demonstrated that increased dietary calcium alleviates the mitogenic effect of a cholic acid supplemented diet on the colonic epithelium.

Animals↗
PubMed1993

Cholic acid and ursodeoxycholic acid therapy in primary biliary cirrhosis. Changes in bile acid patterns and their correlation with liver function.

We treated 6 patients with Stage II primary biliary cirrhosis with cholic acid (CA) 10 mg.kg-1 per day for 3 months and then with the same dose of ursodeoxycholic acid (UDCA). A matching group of 6 patients was observed for 3 months without any therapy. Liver function tests and serum and stool bile acids were investigated before, during and at the end of CA and UDCA therapy. The results of liver function tests deteriorated after 6-8 weeks of CA therapy and the changes were correlated (r = 0.92) with an increase in alpha-dihydroxy-bile acids (chenodeoxycholic acid and deoxycholic acid) in the serum. The 24 h excretion of DCA in 24 h faeces was markedly increased. Ursodeoxycholic acid treatment improved liver function tests; after 4 weeks glutamate dehydrogenase (GLDH) had decreased. After 8-12 weeks of therapy ursodeoxycholic acid had increased to 50-60% of the total serum bile acids whereas the more apolar bile acids were significantly decreased. No changes in liver function tests or bile acid metabolism were found in the untreated group. Since CA and UDCA are non-toxic in man, this trial indicates that the apolar bile acids chenodeoxycholic acid and deoxycholic acid may be responsible for the deterioration of liver function in primary biliary cirrhosis. However, the therapeutic effect of UDCA cannot be explained merely by the decrease in alpha-dihydroxy-bile acids in the serum, since the laboratory results had improved prior to the decrease in the serum apolar bile acids.

Bile Acids and Salts↗
PubMed1982

[Value of serum levels of conjugated cholic acid in the diagnosis of liver disease (author's transl)].

Serum concentrations of conjugated cholic acid determined radioimmunologically were investigated for 3 hours after a test meal in 62 patients with fatty liver, 70 patients with chronic hepatitis and 30 patients with liver cirrhosis. Values were compared with results of further data from chemical pathology. Increased fasting bile acid values were found in 18% of patients with fatty liver, 13% with chronic hepatitis and in 70% with cirrhosis. Following the test meal maximum concentration increase of cholic acid conjugates was obtained after one hour. 70.5% of patients with fatty liver, 80% of patients with chronic hepatitis and 97% of patients with cirrhosis were identifiable by increased bile acid levels. Postprandial serum bile acid levels therefore have a higher sensitivity for diagnosis of liver disease than bilirubin, glutamic-oxaloacetic transaminase, alkaline phosphatase or gamma-glutamyl transferase.

Adult↗
PubMed1980

Effects of cholic acid on the metabolism of endogenous plasma triglyceride and on biliary lipid composition in hyperlipoproteinemia.

Plasma lipids, endogenous triglyceride kinetics, and biliary lipid composition were determined in 13 patients with primary hyperlipoproteinemia (HLP) before and during treatment with cholic acid (15 mg/kg body weight/day for 3 months). In patients with type IIa HLP (n = 5), no consistent effects were seen on fasting plasma lipids or triglyceride turnover determined over a 10-hour period. Plasma triglyceride concentration was decreased in six of the eight patients with type IV HLP. Apparent triglyceride production rate was not significantly changed with initially elevated triglyceride synthesis. Treatment with cholic acid resulted in an increased proportion of bile acids and a decreased proportion of cholesterol and phospholipids in fasting duodenal bile; bile saturation with cholesterol was not significantly reduced. The results ,re discussed in relation to previous studies on the integrated regulation of bile acid and triglyceride metabolism, and it is concluded that cholic acid and chenodeoxycholic acid exert different effects on plasma triglyceride metabolism and on biliary lipid composition in HLP.

Adult↗
PubMed1981

Competitive inhibition of the uptake of demethylphalloin by cholic acid in isolated hepatocytes. Evidence for a transport competition rather than a binding competition.

Cholic acid inhibits the uptake of demethylphalloin (DMP), in a competitive manner. The bile acid increases the Michaelis constant but not Vmax of the inward transport. The inhibition constant Ki for cholate was found to be 8 microM. Cholate competes for the transport system but not for intracellular binding of phallotoxins. Various experimental data presented in this paper exclude an accumulation of phallotoxins in hepatocytes by intracellular binding only. Preincubation of hepatocytes with small concentration of either (3H)-demethylphalloin or (14C)-cholate and subsequent treatment with high concentrations of the non-labelled compounds reduces the intracellular concentration of both radioactive substrates. In accordance with earlier findings the above results suggest a common component needed for the transport of both phallotoxins and cholic acid.

Alkaloids↗
PubMed1994

A single intravenous high dose of cholic acid to a pregnant ewe does not affect fetal well-being.

Cardiovascular variables of both mother and fetus and total bile acid levels were monitored in amniotic fluid and in maternal and fetal plasma after the administration of a single intravenous high dose (29 mg) of cholic acid to a pregnant ewe. We observed the diffusion of significant quantities of cholic acids from the mother to the fetus and amniotic fluid. Nevertheless, cardiovascular parameters (heart rate, blood pressure, PO2, PCO2 and pH) were not affected, neither did intra-amniotic pressure show significant changes compared with the initial experimental conditions. It is concluded that an acute increase in maternal plasma levels of bile acids does not produce important adverse effects in either the mother animal or the fetus and consequently, if bile acids should be deemed responsible for any deleterious effect observed in a preterm fetus in intrahepatic cholestasis, this should be considered as the consequence of a chronic process.

Animals↗
PubMed1983

The degradation of cholic acid by Pseudomonas sp. N.C.I.B. 10590 under anaerobic conditions.

The bacterial degradation of cholic acid under anaerobic conditions by Pseudomonas sp. N.C.I.B. 10590 was studied. The major unsaturated neutral compound was identified as 12 beta-hydroxyandrosta-4,6-diene-3,17-dione, and the major unsaturated acidic metabolite was identified as 12 alpha-hydroxy-3-oxochola-4,6-dien-24-oic acid. Eight minor unsaturated metabolites were isolated and evidence is given for the following structures: 12 alpha-hydroxyandrosta-4,6-diene-3,17-dione, 12 beta,17 beta-dihydroxyandrosta-4,6-dien-3-one, 12 beta-hydroxyandrosta-1,4,6-triene-3,17-dione, 12 beta,17 beta-dihydroxyandrosta-1,4,6-trien-3-one, 12 beta-hydroxyandrosta-1,4,6-triene-3,17-dione, 12 beta,17 beta-dihydroxyandrosta-1,4,6-trien-3-one, 12 alpha-hydroxyandrosta-1,4-diene-3,17-dione, 3-hydroxy-9,10-secoandrosta-1,3,5(10)-triene-9,17-dione, 3,12-dioxochola-4,6-dien-24-oic acid and 12 alpha-hydroxy-3-oxopregna-4,6-diene-20-carboxylic acid. In addition, a major saturated neutral compound was isolated and identified as 3 beta,12 beta-dihydroxy-5 beta-androstan-17-one, and the only saturated acidic metabolite was 7 alpha,12 alpha-dihydroxy-3-oxo-5 beta-cholan-24-oic acid. Nine minor saturated neutral compounds were also isolated, and evidence is presented for the following structures: 12 beta-hydroxy-5 beta-androstane-3,17-dione, 12 alpha-hydroxy-5 beta-androstane-3,17-dione, 3 beta,12 alpha-dihydroxy-5 beta-androstan-17-one, 3 alpha,12 beta-androstan-17-one, 3 alpha,12 alpha-dihydroxy-5 beta-androstan-17-one, 5 beta-androstane-3 beta,12 beta,17 beta-triol, 5 beta-androstane-3 beta,12 alpha,17 beta-triol, 5 beta-androstane-3 alpha,12 beta,17 beta-triol and 5 beta-androstane-3 alpha,12 alpha,17 beta-triol. The induction of 7 alpha-dehydroxylase and 12 alpha-dehydroxylase enzymes is discussed, together with the significance of dehydrogenation and ring fission under anaerobic conditions.

Anaerobiosis↗
PubMed1978

Investigations into the choice of immunogen, ligand, antiserum and assay conditions for the radioimmunoassay of conjugated cholic acid.

Investigations into the choice of immunogen, ligand, antiserum and assay conditions for the radioimmunoassay of conjugated cholic acid have been performed with a view to producing optimal assay conditions. Cholic acid-BSA was found to be the best immunogen to produce antibodies to conjugated cholic acid and the response was of an IgG type. Incorporating a spacer (hexanoic acid) between hapten and carrier protein resulted in a decrease in antiserum titre. Optimal conditions for the assay were found using [125I]histamine-glycocholic acid as ligand with a dilution of antiserum to produce 60% binding of ligand and a pH of 7.4. Using these assay conditions no serum effects were found; extraction of serum prior to assay was therefore unnecessary. The assay was sensitive enough to detect post-prandial increased in serum bile acid concentrations following a liquid test meal; no increase was observed throughout the same time period in a fasting control.

Antibody Specificity↗
PubMed1980

Determination of duodenogastric reflux by use of 14C-labelled cholic acid. An experimental study in dogs.

A method for determination of duodenogastric reflux was elaborated in animal experiments. The bile acid pool was labelled by intravenous injection of 14C-cholic acid and the activity in consecutively collected gastric samples was determined. The gastric samples were taken approximately 24 hours after injection of the tracer. In one dog, provided with a continent duodenostomy, the radioactivity in duodenal samples was found to vary moderately 24-32 hours after injection of labelled cholic acid. The method was tested in three different groups of dogs: a) "normal dogs", B) dogs having undergone partial gastric resection (B I), and C) dogs provided with a reflux-preventing valve after partial gastric resection. Radioactivity was measured in gastric samples from one out of 15 normal dogs and in samples from 11 out of 13 dogs after partial gastric resection. After interposition of a reflux-preventing valve, no radioactivity was found in samples from six tested dogs. Measurement of radioactivity in gastric samples collected approximately 24 hours after labelling of the bile acid pool seems to be a reliable and simple method for semi-quantitative determination of duodenogastric reflux.

Animals↗
PubMed2005

SNPs (single nucleotide polymorphisms) detection based on the formation of cholic-acid binding DNA aptamer.

Simple and rapid methods for the detection of single nucleotide polymorphisms (SNPs) are required to analyze the genetic information. We have previously isolated DNA aptamers that bind to cholic acid by an in vitro selection method. A common feature of the sequences of the aptamers was that they included a secondary structure, a three-way junction, in which three stems were connected at the junction. It was also revealed that three-way junctions with fully matched three stems bind cholic acid whereas single-base substitutions at the junction lose binding affinity completely. Here we report a new method for the detection of single nucleotide mutations that is based on the formation of fully matched three-way junctions which bind to cholic acid.

Aptamers, Nucleotide↗
PubMed2001

Anodic electrochemical oxidation of cholic acid.

Regioselectivity in the anodic electrochemical oxidation of cholic acid with different anodes is described. The oxidation with PbO(2) anode affords the dehydrocholic acid in quantitative yield after 22 h. 3alpha,12alpha-Dihydroxy-7-oxo-5beta-cholan-24-oic acid (59%) and 3alpha-hydroxy-7,12-dioxo-5beta-cholan-24-oic acid (51%) are obtained stopping the reaction at lower time. The rate of the OH-oxidation is C7 > C12 > C3. The electro-oxidation with platinum foil anode gives selectively the 7-ketocholic acid in 40% yield. On the other hand, the graphite plate anode, varying the reaction conditions, produces selectively the dehydrocholic acid in quantitative yield or the 3alpha,12alpha-dihydroxy-7-oxo-5beta-cholan-24-oic acid (96%) while the 3alpha,7alpha-dihydroxy-12-oxo-5beta-cholan-24-oic acid (34%) is obtained together with the other oxo acids.

Cholic Acid↗
PubMed1981

The effect of continuous enteral feeding on cholic acid kinetics in a child.

Continuous enteral feeding is utilized for nutritional support and specific therapy for several pediatric diseases, including protracted infantile diarrhea. Its effects on the enterohepatic circulation of bile acids were studied in a boy during continuous intragastric feeding of a high fat diet at age 42 months and after recovery while on bolus feedings at age 51 months. Cholic acid kinetics measured by the isotopic dilution technique using cholic-COOH-14C acid and meal stimulated intraluminal bile acid concentrations were measured. Cholic acid pool size was unaltered (1294 mg/m(2)) during continuous feeding compared to 999 mg/m(2) during bolus feeds and 1072 plus or minus 243 mg/m(2) (mean plus or minus SE) in nine control children. However, the cholic acid fractional turnover rate was increased 3-fold (0.912 days(-1)) during continuous feeds compared to 0.309 days(-1) during bolus feeding and 0.365 plus or minus 0.163 in controls. Similarly, synthesis rate was increased 3-4 fold during continuous feeds (1180 mg/m(2)/day) compared to controls (363 plus or minus 193 mg/m(2)/day) and the patient during bolus feeding (309 mg/m(2)/day). The intraluminal bile salt concentration was apparently reduced both during treatment (3.86 mM) and when bolus fed (3.85 mM) but were significantly different from controls (7.12 plus or minus 1.74 mM). During continuous enteral feeding with a high fat diet, effective homeostatic mechanisms in the enterohepatic circulation of bile salts ensured intraluminal bile salt concentrations adequate for normal fat solubilization and, consequently, normal fat absorption.

Bile↗
PubMed1977

Comparison of the effects of cholic acid and chenic acid feeding on rates of cholesterol synthesis in the liver of the rat.

To compare the ability of cholic acid and chenic acid to suppress cholesterol synthesis in the liver, these two bile acids were fed in varying amounts to rats for either 66 hr or 6 weeks. In both instances there were significant changes in the bile acid pool in the small intestine and suppression of the rate of cholesterol synthesis in the liver. The administration of cholic acid, however, consistently produced greater suppression of the rate of cholesterol synthesis from octanoate or of microsomal HMG CoA reductase activity than did the administration of a similar amount of chenic acid. Furthermore, this difference was present whether the rates of cholesterogenesis were measured at high-substrate concentrations, ie, under conditions where Vmax was apparently achieved, or under circumstances where there was essentially no extracellular substrate present. These findings do not support the view that the superiority of chenic acid for dissolution of gallstones is secondary to its greater effect as an inhibitor of hepatic cholesterol synthesis.

Animals↗
PubMed2000

Alpha 1-fetoprotein transcription factor is required for the expression of sterol 12alpha -hydroxylase, the specific enzyme for cholic acid synthesis. Potential role in the bile acid-mediated regulation of gene transcription.

Cholesterol conversion to bile acids occurs via the "classic" (neutral) or the "alternative" (acidic) bile acid biosynthesis pathways. Sterol 12alpha-hydroxylase/CYP8b1 is the specific enzyme required for cholic acid synthesis. The levels of this enzyme determine the ratio of cholic acid to chenodeoxycholic acid and thus the hydrophobicity of the circulating bile acid pool. Expression of the 12alpha-hydroxylase gene is tightly down-regulated by hydrophobic bile acids. In this study, we report the characterization of two DNA elements that are required for both the 12alpha-hydroxylase promoter activity and bile acid-mediated regulation. Mutation of these elements suppresses 12alpha-hydroxylase promoter activity. Mutations of any other part of the promoter do not alter substantially the promoter activity or alter regulation by bile acids relative to the wild type promoter. These two DNA elements bind alpha(1)-fetoprotein transcription factor (FTF), a member of the nuclear receptor family. We also show that overexpression of FTF in a non-liver cell line activates the sterol 12alpha-hydroxylase promoter. These studies demonstrate the crucial role of FTF for the expression and regulation of a critical gene in the bile acid biosynthetic pathways.

Animals↗
PubMed1988

Superoxide dismutase activity during dimethylhydrazine colon carcinogenesis and the effects of cholic acid and indole.

Copper, zinc superoxide dismutase (Cu,ZnSOD) and manganese superoxide dismutase (MnSOD) activities were measured in mouse large intestinal mucosa during dimethylhydrazine (DMH) carcinogenesis. Mice were divided into five groups. Group A was subcutaneously injected with DMH (20 mg/kg) weekly and fed with a diet containing 0.2% cholic acid (C) and 0.8% indole (I). Group B was injected with DMH and given indole feeding. Group C was treated with DMH injection and cholic acid feeding. Group D was given DMH injection alone. Group E was an age-matched control group given 0.9% NaCl injection. The experiment last 21 weeks. The Cu, ZnSOD activity of intestinal mucosa in group A animals began to increase significantly at the 7th week of the experiment. In groups B, C and D, however, this enzyme was not elevated statistically until the 16th week, and then each of these groups kept an increased Cu,ZnSOD level the rest of the experimental period. MnSOD activity was elevated statistically in group C animals at the 7th week. The enzyme activity in group A and D animals increased at the 9th week, but the enzyme activity did not increase statistically until the 11th week in group B. After the 16th week of the experiment the increased activity of MnSOD in all experimental groups returned to the level of the control group. Large intestinal cancer tissues had increased Cu,ZnSOD activity and decreased MnSOD activity.

Adenocarcinoma↗
PubMed1992

Reduction of cardiovascular and thyroxine-suppressing activities of L-T3 by liver targeting with cholic acid.

This study was designed to determine whether the conjugation product of L-T3 with cholic acid would result in a liver-targeted compound (CGH 509A) with hypocholesterolemic (HC) activity significantly dissociable from cardiovascular (CV) and thyroxine-suppressing (TS) effects normally observed with thyroid hormone. Evaluation of HC activity in lipemic rats showed that CGH 509A was 6 times less potent than L-T3 with ED25 values estimated at 150 and 25 nmol/kg, respectively. CV function measured as changes in atrial rate, atrial tension and heart weight was determined in euthyroid rats. CGH 509A was at least 64 times less cardio-stimulant than L-T3 with minimum effective doses estimated at 2350 and 37 nmol/kg, respectively. TS activity was assessed in euthyroid rats as the potency of any compound to reduce plasma T4 levels. CGH 509A was 50 times less potent than-L-T3 with ED50 values estimated at 900 and 18 nmol/kg, respectively. From these results, it is clear that, while L-T3 was equally potent on HC, CV and TS activities, the HC potency of CGH 509A was at least 15 and 6 times greater than its CV and TS potencies, respectively.

Animals↗