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Results for “CHOLIC ACID”

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PubMed1976

Effect of Beta-sitosterol on cholesterol-cholic acid-induced gallstone formation in mice.

Beta-sitosterol has been shown to prevent gallstone formation in mice fed 1.2% cholesterol and 0.5% cholic acid (lithogenic diet). The incidence of gallstone formation in the mouse by the addition of 2.5% sitosterol in the lithogenic diet is about 35.5% in male and 25% in female. The condition of the liver, whether fatty or normal, did not correlate with the presence or absence of cholelithiasis. The serum and liver cholesterol levels of mice fed either sitosterol and cholesterol or sitosterol and cholic acid is lower than those of mice fed cholesterol or cholic acid alone. Elevation of liver phospholipid concentration was noticed in mice fed sitosterol or a combination of sitosterol with cholesterol or cholic acid or both cholesterol and cholic acid.

Animal Feed↗

PubMed1980

The effect of bile acids and lipase on absorption of tallow in young chicks.

White leghorn chicks were fed diets with 4% tallow supplemented with one of the following bile acids at .04%: cholic acid, chenodeoxycholic acid, dehydrocholic acid, deoxycholic acid, or sodium taurocholate. Cholic acid improved the absorption of tallow but not significantly; chenodeoxycholic acid significantly improved tallow absorption during days 0 to 7 but decreased it during days 14 to 21. The bile acids, dehydrocholic acid, deoxycholic acid, and sodium taurocholate had no significant effect on absorption of tallow. In a 2 x 3 factorial design involving cholic acid and lipase, .04% cholic acid and/or .10% lipase significantly improved the absorption of tallow by 8 and 4% in chicks 1 and 3 weeks of age, respectively. Dry matter digestibility and efficiency appeared to be improved with the improvement of lipid absorption.

Animals↗

PubMed2003

Gene structure of pig sterol 12alpha-hydroxylase (CYP8B1) and expression in fetal liver: comparison with expression of taurochenodeoxycholic acid 6alpha-hydroxylase (CYP4A21).

Cholic acid is the major trihydroxy bile acid formed in most mammals. The domestic pig (Sus scrofa) is an exception. The bile of adult pig is devoid of cholic acid whereas hyocholic acid is found in amounts equal to that of cholic acid in humans. The pathway leading to formation of hyocholic acid is believed to be species-specific and to have evolved in the pig to compensate for a nonexistent or deficient cholic acid biosynthesis. However, a high level of cholic acid has recently been found in the bile of fetal pig. Here we describe that a gene encoding the key enzyme in cholic acid biosynthesis, the sterol 12alpha-hydroxylase (CYP8B1), is in fact present in the pig genome. The deduced amino acid sequence shows 81% identity to the human and rabbit orthologues. CYP8B1 mRNA is expressed at significant levels in fetal pig liver. Both CYP8B1 and the key enzyme in hyocholic acid formation, taurochenodeoxycholic acid 6alpha-hydroxylase (CYP4A21), were found to be expressed in pig liver in a developmental-dependent but opposite fashion.

Adult↗

PubMed1993

Selectivity and sensitivity of changes in serum bile acids during induction of cirrhosis in rats.

Because some patients with cirrhosis have serum transaminase levels within the normal range, a prospective study was undertaken to determine whether the concentration of individual serum bile acids would be a sensitive indicator of development of cirrhosis. The choline-deficient rat has been used as a model for study of these changes. Using high-performance liquid chromatography, we measured the concentrations of individual serum bile acids at 3, 6, 10, 20 and 30 wk of dietary intake. Serum levels of total glycine- and taurine-conjugated bile acids were elevated at all stages tested as compared with levels in control groups (choline supplemented). Similarly, unconjugated bile acids and, particularly, cholic acid showed significantly higher levels at all stages except with the occurrence of cirrhosis at 30 wk, at which time there was a significantly lower level for unconjugated bile acids (0.48 +/- 0.11 vs. 1.40 +/- 0.36 in controls) and for cholic acid (0.17 +/- 0.05 vs. 0.91 +/- 0.39 in controls). The ratio of serum cholic acid to serum chenodeoxycholic acid changed in temporal relationship to progression in the histological lesions in livers of these rats. The ratio was at its highest at 78 +/- 3 at 3 wk (no histological change) and decreased with increasing time and changes in histological appearance until 30 wk, at which time it was down to 1.6 +/- 0.6. The routinely used markers of liver injury (serum ALT, alkaline phosphatase and bilirubin), however, did not match the progression of hepatic histological changes.(ABSTRACT TRUNCATED AT 250 WORDS)

Alanine Transaminase↗

PubMed1980

Analysis of plasma bile acid profiles in patients with liver diseases associated with cholestasis.

Bile acids in plasma of patients with intra- or extra-hepatic cholestasis have been analyzed by gas chromatography-mass spectrometry after fractionation into groups by mode of conjugation. During cholestasis plasma concentrations ranged from 14 to 252 mumol/l. The predominant bile acid was cholic acid, comprising 44% to 89% of total bile acids. Tetrahydroxy- and trihydroxy-cholanoates with a tentative 6-hydroxy structure were identified, whereas 1-hydroxylated bile acids were not found. 3 beta-Hydroxy-5-cholenoic acid was the most important monohydroxycholanoate, comprising up to 13% of total bile acids in serum. The ratio of cholic to chenodeoxycholic acid in patients with primary biliary cirrhosis was in all cases more than 1. With the exception of 1-hydroxylated bile acids the main bile acids in urine an plasma were the same. Renal clearance of individual conjugated and sulfated bile acids could be calculated for some of the patients, assuming insignificant metabolism of bile acids in the kidney. The renal clearance of cholic acid conjugates tended to be higher tna that of chenodeoxycholic acid conjugates, and sulfates of cholic acid conjugates tended to have a higher renal clearance than sulfates of chenodeoxycholic acid conjugates. The clearance of sulfated 3 beta-hydroxy-5-cholenoic acid was still smaller. Chenodeoxycholic acid predominated in two healthy persons. Unconjugated bile acids accounted for 30% and 53%, respectively, of total bile acids. Sulfates of lithocholic, allolithocholic, and 3 beta-hydroxy-5-cholenoic acids were found after stimulation with a test meal.

Adult↗

PubMed1989

The effects of intraduodenal bile acid administration on biliary secretion of ionized calcium and carbonate in man.

The importance of calcium in gallstone formation is increasingly recognized. Calcium carbonate is an important constituent of gallbladder stones and may be present in the nidus of cholesterol stones. Secondary deposition of calcium carbonate on the surface of cholesterol gallstones is an important reason for failure of oral bile acid dissolution therapy. We sought to determine the effects of bile acids on the crystallization conditions of calcium carbonate in bile. We studied 18 patients with choledocholithiasis with a percutaneous or endoscopically placed catheter high in the biliary tree. Samples of bile in the basal state and following replacement of the bile acid pool with cholic acid, chenodeoxycholic acid and ursodeoxycholic acid were analyzed for total calcium, ionized calcium, bicarbonate and carbonate, and the saturation index for calcium carbonate was calculated. Hepatic bile in the basal state was supersaturated with calcium carbonate. Total calcium concentrations rose linearly with rising bile acid concentrations but ionized calcium was maintained in a relatively narrow range. These data are consistent with an important role for bile acids in binding calcium. Extrapolation of the linear regressions between bile acid concentration and calcium concentrations suggested that in the absence of bile acids, biliary calcium concentrations are in passive equilibrium with plasma. Chenodeoxycholic acid and ursodeoxycholic acid caused a bicarbonate-rich choleresis and significantly augmented the saturation index for calcium carbonate, whereas cholic acid caused no change. In contrast with animal models, the apparent choleretic activity of cholic acid, chenodeoxycholic acid and ursodeoxycholic acid was similar, and no hyper-choleresis was observed with ursodeoxycholic acid. Chenodeoxycholic acid and ursodeoxycholic acid therefore increase the thermodynamic possibility for calcium carbonate precipitation.

Aged↗

PubMed1977

Effect of type and amount of dietary fat and 1,2-dimethylhydrazine on biliary bile acids, fecal bile acids, and neutral sterols in rats.

The effect of type (corn oil or lard) and quantity (5 or 20%) of dietary fat and 1,2-dimethylhydrazine (DMH) on the composition of biliary bile acids, fecal bile acids, and neutral sterols was studied in rats exposed to a given regimen for two generations prior to s.c. treatment with DMH for 20 weeks. Biliary excretion of total bile acids as well as cholic acid, beta-muricholic acid, ursodeoxycholic acid, and deoxycholic acid was higher in rats fed a diet containing 20% corn oil or lard than it was in rats fed diets containing 5% corn oil or lard. Treatment of animals with DMH produced an increase in biliary total bile acids, cholic acid, hyodeoxycholic acid, and deoxycholic acid irrespective of diets. High-fat (corn oil or lard at 20% level) intake was associated with an increased excretion of fecal neutral sterols and bile acids. The excretion of deoxycholic acid, lithocholic acid, and 12-ketolithocholic acid was increased in rats fed high-fat diets. The source of fat had no major influence on the excretory pattern of cholesterol metabolites and bile acids. DMH-treated animals excreted higher levels of fecal coprostanol, coprostanone, deoxycholic acid, lithocholic acid, and 12-ketolithocholic acid than did controls.

Animals↗

PubMed1984

7 alpha-Dehydroxylation of bile acids by resting cells of a Eubacterium lentum-like intestinal anaerobe, strain c-25.

7 alpha-Dehydroxylation of cholic acid and chenodeoxycholic acid by whole cells of strain c-25, a Eubacterium lentum-like intestinal anaerobe, was studied. 7 alpha-Dehydroxylase activity was observed only in whole cells grown in the presence of the primary bile acid (cholic acid or chenodeoxycholic acid). Chenodeoxycholic acid was twice as effective as cholic acid as an inducer. Although cells grown in the presence of chenodeoxycholic acid had no significant substrate specificity for the two primary bile acids, cells grown in the presence of cholic acid showed two times greater activity against cholic acid than chenodeoxycholic acid. Exposure of cell suspensions to atmospheric oxygen resulted in little loss of the 7 alpha-dehydroxylase activity. The induced enzyme had an optimal pH range of 7.3 to 7.7. Although adding flavin mononucleotide to the growth medium significantly increased the 7 alpha-dehydroxylation of bile acids without an increase in cell growth, inhibition of the enzyme activity was observed in the resting cell system when flavin mononucleotide was included in the reaction mixture.

Animals↗

PubMedDate not supplied

Bile acids and bile alcohols in two patients with Zellweger (cerebro-hepato-renal) syndrome.

The Zellweger cerebro-hepato-renal syndrome (CHRS) is a rare hereditary disease in which there is a generalized deficiency of peroxisomal function. Liver peroxisomes are important for the conversion of 3 alpha,7 alpha,12 alpha-trihydroxy-5 beta-cholestanoic acid into cholic acid, and, consequently, 3 alpha,7 alpha,12 alpha-trihydroxy-5 beta-cholestanoic acid and metabolites of this bile acid precursor accumulate in serum and bile of patients with CHRS. Little is known about the urinary excretion of bile acids in this disease. Using gas chromatography-mass spectrometry we have analyzed serum bile acids and urinary excretion of bile acids and bile alcohols in two Swiss male CHRS patients. As expected, serum concentrations and urinary excretions of 3 alpha,7 alpha,12 alpha-trihydroxy-5 beta-cholestanoic acid and 3 alpha,7 alpha,12 alpha,24-tetrahydroxy-5 beta-cholestanoic acid were elevated, which is probably an obligatory finding in CHRS. In addition, the urinary excretion of 1,3,7,12-tetrahydroxy-5 beta-cholanoic acid (a very polar unusual bile acid) was increased (99-1556 nmol/24 h). In contrast, the excretion of the major urinary bile alcohol, 27-nor-5 beta-cholestane-3 alpha, 7 alpha,12 alpha,24,25-pentol was found to be normal. 3 alpha, 7 alpha,12 alpha-Trihydroxy-5 beta-C29-dicarboxylic acid, a metabolite of 3 alpha,7 alpha,12 alpha-trihydroxy-5 beta-cholestanoic acid previously believed to be obligatory in CHRS, was found only in one of our patients.

Abnormalities, Multiple↗

PubMed1985

Intestinal absorption and metabolism of norcholic acid in rats.

Intestinal absorption and hepatic and intestinal bacterial biotransformations of norcholic acid, the C23 homologue of cholic acid, were studied in the rats. Norcholic acid, like cholic acid, was efficiently absorbed from the intestine and quickly secreted into the bile. Unlike the C24 bile acid, however, which is secreted by rat liver as its taurine conjugate, the C23 bile acid appeared in the bile predominantly as the unconjugated form. conjugated form. Bacterial modification of norcholic acid was similar to but less extensive than that of cholic acid. A considerable part of norcholic acid was left unchanged during its passage through the intestinal tract. A major bacterial metabolite of norcholic acid was the 7-dehydrogenation product, 7-ketonordeoxycholic acid, rather than the 7-dehydroxylation product, nordeoxycholic acid, though the reverse is true for cholic acid.

Animals↗

PubMed2001

Activities of cholic acid-derived antimicrobial agents against multidrug-resistant bacteria.

Cationic cholic acid derivatives displayed potent and broad-spectrum activity against multidrug-resistant Gram-negative and -positive bacteria. Specific examples were effective permeabilizers of the outer membranes of many strains of multidrug-resistant Gram-negative bacteria and sensitized these to hydrophobic antibiotics. We also prepared a new cholic acid derivative with improved apparent selectivity for prokaryote membranes.

Anti-Bacterial Agents↗

PubMedDate not supplied

Bile acid synthesis in young and old rats.

Bile acid synthesis from orally administered (14)C-cholesterol or from (14)C-mevalonic acid administered intravenously were examined in male and female 2-, 12- and 24-month-old rats. About 5-9% of the '4C-cholesterol administered was recovered as bile acids from the small intestine 3 days after administration. The value in the case of (14)C-mevalonic acid was about 1/10 that of (14)C-cholesterol. Major bile acids were cholic acid and beta-muricholic acid, and the formation ratio of cholic acid increased in aged rats, although no further difference was found between 12- and 24-month-old animals of either sex. Male rats formed more beta-muricholic acid than females at all ages examined. In addition, no significant difference was found in the bile acid composition between both precursors, (14)C-cholesterol and (14)C-mevalonic acid.

Journal Article↗

PubMed1985

Effect of bile acids on formation of the mutagen, quercetin, from two flavonol glycoside precursors by human gut bacterial preparations.

Human fecal cultures, induced with either of the flavonols, quercitrin or rutin, were grown in the presence of various concentrations of chenodeoxycholic acid, deoxycholic acid or cholic acid. Cell-free preparations (fecal preparations) from these cultures were then incubated with rutin or quercitrin. The formation of the aglycone, quercetin, was monitored by the Ames assay using tester strain TA98. The presence of chenodeoxycholic or deoxycholic acids in the quercitrin-induced culture resulted in a fecal preparation which enhanced the mutagenesis of quercitrin approximately two-fold at optimal concentrations of 0.6 mM and 0.8 mM respectively. Higher concentrations of these bile acids decreased the activity of the fecal preparations. Cholic acid gave similar results except a much higher concentration (3.0 mM) was required to achieve this effect. Analogous results with rutin-induced cultures were less clear cut: considerable variation in bile acid effect was noted among volunteers. The authors propose that bile acid in the medium may enhance the ability of rutin- and quercitrin-glycosidase elaborating organisms to successfully compete with other microbial populations. Additionally, the greater variation in results using rutin as inducer may reflect more heterogeneous populations of organisms active against this substrate. The possible role of bile acids and flavonols in bowel cancer is discussed.

Adult↗

PubMed1975

Bile acids. XLIV, quantitation of bile acids from the bile fistula rat given (4-14C) cholesterol.

The bile acids derived from [4-14-C]cholesterol administered intracardially to rats with cannulated bile ducts were identified and quantitated. Over a period of 28 days about 90% of the administered 14-C was found in bile of which 73% was retained in the biliary acid fraction. [7beta-3-H]cholic acid, alpha-muri[3beta-3-H]cholic acid, beta-muri[3beta-3-H]cholic acid and litho[3beta-3-H]cholic acid were prepared with specific activities of about 30 muCi/mg by reduction of appropriate ketonic precursors with NaB3H4 and were added to the biliary acid fraction. After separation and purification of the bile acids, cholic, chenodeoxycholic, alpha- and beta-muricholic acids accounted for 70, 16, 7.5 and 6.1%, respectively, of the 14-C in the biliary acid fraction. The specific activities of these isolated 14-C-labeled acids were almost identical. Lithocholic acid accounted for a maximum of 0.2% and ursodeoxycholic acid and 7-oxolithocholic acid could account for no more than 2% of the biliary 14-C. Gas-liquid chromatography on 3% OV-17 of the trimethylsilyl ether derivatives of the methyl esters of the common bile acids of rat bile results in their complete separation and provides a convenient means of estimating the relative proportions of these acids in rat bile. By this method, the relative amounts of the four major acids, cholic, chenodeoxycholic, alpha- and beta-muricholic acids were 63, 20, 8 and 6%, respectively.

Animals↗

PubMed1991

Vasoconstrictive effect of bile acids on isolated human placental chorionic veins.

Intrahepatic cholestasis of pregnancy (ICP) is a rare complication of late pregnancy associated with a high rate of premature delivery, antepartum fetal death and fetal hypoxia. Since the principal biochemical feature of ICP is a marked elevation of maternal serum bile acid levels, a role of these substances in the pathophysiology of fetal complications has been suggested. In this study, the effect of bile acids on isolated human placental chorionic veins is described. High concentrations of bile acids, especially cholic acid, have a dose-dependent vasoconstrictive effect, which suggests that these substances could exert a detrimental effect on the fetus by increasing the resistance in chorionic veins through a vasospasm of the placental chorionic surface. An abrupt reduction of the oxygenated blood flow at the level of the placental chorionic plate may cause an acute impairment of the fetal perfusion and oxygenation, leading to fetal asphyxia. This is the first report that provides experimental evidence of the possible role of bile acids in those mechanisms that trigger fetal asphyxia in pregnancies complicated by ICP.

Bile Acids and Salts↗

PubMed1995

Profile of urinary bile acids in familial intrahepatic cholestasis with Coombs' negative haemolytic anaemia.

We present two male siblings with intrahepatic cholestasis and prolonged indirect hyperbilirubinaemia. Their familial intrahepatic cholestasis syndrome was characterized by Coombs' negative haemolytic anaemia, without giant cell transformation of hepatocytes and high concentrations of serum gamma-glutamyl transpeptidase and cholesterol. By gas chromatography-mass spectrometry, we detected large amounts of 1 beta-hydroxylated bile acids, especially 1 beta,3 alpha,7 alpha,12 alpha-tetrahydroxy-5 beta-cholan-24-oic acid (25.5-67.9% of total urine bile acids) in the urine during phenobarbital therapy. However, the amount of urinary 1 beta-hydroxylated bile acids gradually decreased as the disease progressed. At the end-stage, we detected large amounts of 7 alpha,12 alpha-dihydroxy-3-oxochol-4-en-24-oic acid (19.6% of total urine bile acids). The ratio of 7 alpha,12 alpha-dihydroxy-3-oxochol-4-en-24-oic acid to cholic acid in the urine was 0.8. We conclude that in infants with end-stage liver failure, the microsomal hydroxylation of bile acids is impaired and the excretion of delta 4-3-oxo bile acids is increased.

Anemia, Hemolytic↗

PubMed1987

Familial giant cell hepatitis associated with synthesis of 3 beta, 7 alpha-dihydroxy-and 3 beta,7 alpha, 12 alpha-trihydroxy-5-cholenoic acids.

Urinary bile acids from a 3-mo-old boy with cholestatic jaundice were analyzed by ion exchange chromatography and gas chromatography-mass spectrometry (GC-MS). This suggested the presence of labile sulfated cholenoic acids with an allylic hydroxyl group, a conclusion supported by analysis using fast atom bombardment mass spectrometry (FAB-MS). The compounds detected by FAB-MS were separated by thin layer chromatography and high performance liquid chromatography. The sulfated bile acids could be solvolyzed in acidified tetrahydrofuran, and glycine conjugates were partially hydrolyzed by cholylglycine hydrolase. Following solvolysis, deconjugation, and methylation with diazomethane, the bile acids were identified by GC-MS of trimethylsilyl derivatives. The major bile acids in the urine were 3 beta,7 alpha-dihydroxy-5-cholenoic acid 3-sulfate, 3 beta,7 alpha,12 alpha-trihydroxy-5-cholenoic acid monosulfate, and their glycine conjugates. Chenodeoxycholic acid and cholic acid were undetectable in urine and plasma. The family pedigree suggested that abnormal bile acid synthesis was an autosomal recessive condition leading to cirrhosis in early childhood.

3-Hydroxysteroid Dehydrogenases↗

PubMed1998

Contribution of sodium taurocholate co-transporting polypeptide to the uptake of its possible substrates into rat hepatocytes.

As one of the Na+-dependent transporters responsible for the hepatic uptake of ligands, sodium taurocholate (TC) co-transporting polypeptide (NTCP) has been cloned from rat liver and its substrate specificity has been clarified by examining the inhibition of TC uptake mediated by NTCP. The contribution of NTCP to the Na+-dependent uptake of ligands into rat hepatocytes, however, still needs to be clarified. To determine the contribution of NTCP, we examined the uptake of ligands into primary cultured hepatocytes (cultured for 4 h) and into COS-7 cells, transiently expressing NTCP, and normalized the uptake of ligands with TC as a reference compound. Western Blot analysis indicated that NTCP was glycosylated much less extensively in the transfected COS-7 cells, although the expression level was comparable for the cultured hepatocytes and transfectant. Kinetic parameters for the Na+-dependent uptake of TC were similar for the cultured hepatocytes and NTCP-transfected COS-7 cells (Km = 17.7 vs. 17.4 microM; Vmax = 1.63 vs. 1.45 nmol/min/mg protein). Glycocholic acid and cholic acid were taken up by NTCP-transfected COS-7 cells. The contribution of NTCP to the Na+-dependent uptake of glycocholic acid into rat hepatocytes was approximately 80%, whereas that of cholic acid was 40%. In addition, the analysis indicated that the contribution of NTCP to the Na+-dependent uptake of several ligands (ouabain, ibuprofen, glutathione-conjugate of bromosulfophthalein, glucuronide- and sulfate-conjugates of 6-hydroxy-5, 7-dimethyl-2-methylamino-4-(3-pyridylmethyl) benzothiazole) was negligible. Thus, this is a convenient method to determine the contribution of NTCP to the uptake of ligands into hepatocytes. It is also suggested that multiple transport mechanisms are responsible for the Na+-dependent uptake of organic anions into hepatocytes.

Animals↗