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PubMed1987

Free fatty acids in gallstones in mice fed a diet containing cholic acid.

In mice, combined addition of 1% cholesterol and 0.5% cholic acid to a diet induced cholesterol gallstones within 40 days as a result of the supersaturation of cholesterol in the bile, as has been reported. The major component of the gallstone was cholesterol, which was measured by HPLC. In this study, however, single addition of 1% cholic acid to a diet, which did not decrease cholesterol solubilizing capacity in bile, contributed to gallstone formation in mice within 50 days. The gallstones thus formed contained a large amount of palmitic acid. In the hepatic bile of this animal, palmitic acid was also detected; however, no solid material was observed by light and polarized-light microscopes. Free fatty acids such as palmitic acid seem to be dissolved in a complex micelle composed of bile acids and lecithin. This probably causes gallstone formation by reducing cholesterol solubilizing capacity in bile.

Animals↗
PubMed1983

Characteristics of cholic acid uptake in primary cultured hepatocytes.

The characteristics of cholic acid uptake by primary cultured hepatocytes was studied. The cholic acid uptake below 10 degrees C was unsaturable, while that determined at 20 degrees and 37 degrees C showed a biphasic type, which suggested the presence of a saturable process. This saturable process was a temperature-dependent and carrier-mediated transport process with an activation energy of 36.1 Kcal/mol. The apparent Km and Vmax values at 37 degrees C were 57.1 microM and 0.566 nmoles/mg protein/min, respectively. The saturable process was inhibited by 2,4-dinitrophenol and ouabain, and reduced significantly in the absence of sodium, suggesting that this process is energy- and sodium-dependent. The cholic acid uptake mediated by the saturable process in the absence of sodium was, however, significantly larger than that mediated by the unsaturable process. These results suggest that the transport of cholic acid in primary cultured hepatocytes may consist of three different types: unsaturable, sodium and energy-dependent carrier-mediated, and sodium-independent and energy-dependent processes, respectively. The presence of a common transport carrier for cholic acid and its conjugates with taurine and glycine in primary cultured hepatocytes was also suggested.

Animals↗
PubMed1998

Plasma lipoprotein cholesterol levels in rats fed a diet enriched in cholesterol and cholic acid.

To investigate the effects of dietary cholesterol and cholic acid on plasma cholesterol levels, rats fed a cholesterol-free diet or a diet enriched in cholesterol (0.5% or 1%) with or without cholic acid supplementation were studied for 4 weeks. Although 0.5% cholesterol supplementation showed no effect on plasma total cholesterol and LDL-cholesterol levels in rats fed a diet without cholic acid treatment, the addition of dietary cholic acid caused an increase in plasma total cholesterol, LDL-cholesterol and VLDL-cholesterol levels in rats fed a cholesterol-rich diet. There was no significant change in HDL-cholesterol levels among the dietary groups. Rats fed a diet enriched in cholesterol have increased liver total lipids and total cholesterol contents. In addition, lower liver lipid peroxide concentration was found in rats fed a cholesterol-rich diet when compared with those fed the control diet. It is interesting that cholic acid supplementation led to an increase in hepatic cholesterol content and a decrease in liver lipid peroxide concentration in rats fed a cholesterol-rich diet. Results from this study suggest that dietary cholesterol and cholic acid might play an important role in regulation of lipid metabolism in rats.

Administration, Oral↗
PubMed1976

Microbiological degradation of bile acids. The preparation of some hypothetical metabolites involved in cholic acid degradation.

1. To identify the intermediates involved in the degradation of cholic acid, the further degradation of (4R)-4-[4alpha-(2-carboxyethyl)-3aalpha-hexahydro-7abeta-methyl-5-oxoindan-1beta-yl]valeric acid (IVa) by Arthrobacter simplex was attempted. The organism could not utilize this acid but some hypothetical intermediate metabolities of compound (IVa) were prepared for later use as reference compounds. 2. The nor homologue (IIIa) and the dinor homologue (IIIb) of compound (IVa) were prepared by exposure of 3-oxo-24-nor-5beta-cholan-23-oic acid (I) and (20S)-3beta-hydroxy-5-pregnene-20-carboxylic acid (II) to A. simplex respectively. These compounds correspond to the respective metabolites produced by the shortening of the valeric acid side chain of compound (IVa) in a manner analogous to the conventional fatty acid alpha- and beta-oxidation mechanisms. Their structures were confirmed by partial synthesis. 3. The following authentic samples of reduction products of the oxodicarboxylic acids (IIIa), (IIIb) and (IVa) were also synthesized as hypothetical metabolities: (4R)-4-[3aalpha-hexahydro-5alpha-hydroxy-4alpha-(3-hydroxypropyl)-7abeta-methylindan-1beta-yl]valeric acid (Vb) and its nor homologue (VIIa) and dinor homologue (IXa);(4R)-4-[3Aaalpha-hexahydro-5alpha-hydroxy-4alpha-(3-hydroxypropyl)-7abeta-methylindan-1beta-yl]-pentan-1-ol (Vc); and their respective 5beta epimers (Ve), (VIIc), (IXc) and (Vf). 4. In connexion with the non-utilization of compound (IVa) by A. simplex, the possibility that not all the metabolites formed from cholic acid by a certain micro-organism can be utilized by the same organism is considered.

Arthrobacter↗
PubMed1994

Galactosylsucrose and xylosylfructoside alter digestive tract size and concentrations of cecal organic acids in rats fed diets containing cholesterol and cholic acid.

Influences of galactosylsucrose and xylosylfructoside on body mass gain, the digestive tract mass and concentrations of organic acids such as acetic, propionic, butyric, lactic and succinic acid in the cecum were compared among rats fed a cholesterol-enriched fiber-free diet [cholesterol 6 + cholic acid 1.5 (g/kg)] containing either galactosylsucrose, xylosylfructoside or sucrose (100 g/kg) or the above fiber-free diet without test sugar (control) for 21 d. Body mass gain was greater in rats fed sucrose, but not in rats fed galactosylsucrose or xylosylfructoside, than in control rats. The mass of the small intestine and colon plus rectum was larger in rats fed xylosylfructoside than in control rats. Cecal contents and cecal tissue mass were heavier, water content of cecal contents was higher, and pH and ammonia concentration of cecal contents were lower in rats fed diets containing xylosylfructoside than in control rats. Galactosylsucrose had similar effects, although not all differences were significant. The concentration of hydrogen ion in cecal contents positively correlated to total cecal concentration of measured organic acids and to amount of cecal contents. Total concentration of measured organic acids in cecal contents positively correlated to cecal tissue mass. The estimated contribution of galactosylsucrose, xylosylfructoside and sucrose for body mass deposition were 0.19, -0.29 and 0.51 (g body mass gained/g sugar), respectively.

Ammonia↗
PubMed1987

Liver cell membrane solubilization may control maximum secretory rate of cholic acid in the rat.

The factors modulating the maximum secretory rate of cholic acid were investigated. Rats were infused intravenously with cholic acid in measured stepwise increasing doses (1, 2, 3, and 4 mumol X min-1 X 100 g body wt-1). Each dose was infused for 30 min and bile samples were collected every 10 min. Bile flow, bile acid, cholesterol, individual biliary phospholipids, and the fatty acid profiles of the biliary phospholipids were determined. Microsomal and bile canalicular membrane-enriched fractions were isolated from cholic acid-treated rats at the end of the experiment. Membranes were analyzed for cholesterol, phospholipid, and phospholipid fatty acid composition. During cholic acid infusion, the secretion rates of bile acid, cholesterol, phospholipid, and bile flow initially increased and then declined. No evidence of liver cell damage was observed by light or electron microscopy. Maximum phospholipid secretion rate (13.5 nmol X min-1 X g-1) occurred before peak bile flow and bile acid secretory rate maximum (4.72 microliter X min-1 X g-1 and 375 nmol X min-1 X g-1). When phospholipid output declined, the proportion of sphingomyelins and phosphatidylethanolamine relative to phosphatidylcholine increased. This was also reflected in the fatty acid composition. Cholic acid infusion caused a decline in microsomal and bile canalicular membrane phospholipid content without affecting their phospholipid composition. Depletion of membrane phospholipid resulted in an increase in the cholesterol:phospholipid ratio, which is suggested to be the underlying mechanism for modulating cholic acid secretion.

Animals↗
PubMed1994

An improved method for the measurement of total lipid-bound sialic acids after cleavage of alpha 2,8 sialic acid linkage with Vibrio cholerae sialidase in the presence of cholic acid, SDS and Ca2+.

In the measurement of total lipid-bound sialic acids involving periodic acid oxidation, as in the periodate-resorcinol assay, the inner sialic acids of disialoglycolipids (such as GD3 and GD2) are not involved because their alpha 2,8 ketosidic linkages are resistant to periodic acid oxidation, even after acid/enzyme hydrolysis or alkali pretreatment. However, the sialic acids from these glycolipids can be recovered completely after cleavage of alpha 2,8 linkages by V. cholerae sialidase in the presence of cholic acid, sodium dodecyl sulphate and calcium. Interestingly, removal of calcium or detergent(s) or both significantly minimizes the sialidase action on the disialyl residues of these gangliosides. Therefore, we recommend sialidase (Vibrio cholerae) pretreatment of the glycolipids in the presence of cholic acid, SDS and Ca2+ for complete recovery of sialic acids from di- and polysialogangliosides and for accurate measurement of total lipid-bound sialic acids by periodate-resorcinol assay.

Calcium↗
PubMed1981

Effect of the selective expansion of cholic acid pool on bile lipid composition: possible mechanism of bile acid induced biliary cholesterol desaturation.

The effect of cholic acid pool expansion on biliary lipid composition was investigated in 21 subjects with cholesterol gallstones. All subjects were fed cholic acid (15 mg/kg/day) and ampicillin (2 g/day) in order to depress the intestinal degradation of cholic to deoxycholic acid. Five additional subjects were given ampicillin alone. The treatment lasted 2-3 wk. Parameters investigated included biliary and plasma lipid, biliary bile acid composition, and total and individual bile acid pool size. In 11 of 21 subjects (group I) cholic acid pool expanded two-threefold, whereas deoxycholic acid pool increased only slightly. In this group mean saturation index fell from 1.32 +/- 0.27 (mean +/- SD) to 0.93 +/- 0.25 (p less than 0.001), and plasma cholesterol increased from 185 +/- 45 mg/dl before to 213 +/- 37 after treatment (p less than 0.01). In the remaining 10 subjects (group II) the increase of the deoxycholic acid pool for exceeded that of cholic acid, and in these subjects the saturation index rose from a mean value of 1.07 +/- 0.27 to 1.42 +/- 0.22 after treatment (p less than 0.01). In this group plasma cholesterol tended to decrease (from 213 +/- 57 to 197 +/- 51 after treatment). In the 5 subjects treated with ampicillin alone deoxycholic acid pool was greatly reduced, and the saturation index fell from 1.25 +/- 0.25 to 0.95 +/- 0.35. The results suggest that cholic acid pool expansion reduces bile cholesterol saturation, whereas the increase of deoxycholic acid pool tends to supersaturate the bile. It is concluded that a determinant of bile cholesterol saturation might be the detergent power of the bile acid pool.

Adult↗
PubMed2000

In vitro selection of DNA aptamers which bind to cholic acid.

DNA aptamers which bind to cholic acid have been identified by in vitro selection from a pool of approximately 9x10(14) DNA molecules. After 13 rounds of selection, 19 clones with 95-100 nucleotide length were sequenced. Deletion-mutant experiments and computational sequence analysis suggested that all clones contained cholic acid binding sequences which could fold into three-way junction structures. By comparing the sequences involved in the predicted three-way junction structure of these 19 clones, it was determined that the nucleotide sequences and lengths of three stem and loop regions have no similarity. The most conserved structure seems to have three base pairs flanking the junction of the three stems and they may form a hydrophobic cavity in which they interact with cholic acid.

Base Sequence↗
PubMed2003

Dependence of selective enclathration on types of cholic acid crystals.

Competitive recrystallizations of cholic acid (CA) from 1:1 binary mixtures of seven mono-substituted benzenes are demonstrated. The order of preference for guests to be incorporated into the cholic acid crystals are as follows: benzene, toluene > n-amylbenzene, n-hexylbenzene > ethylbenzene, n-propylbenzene, n-butylbenzene. These seven compounds afford bilayer type inclusion crystals that are classified into four types based on the host frameworks and host-guest stoichiometries. The order of selective enclathration corresponds to the four types as follows: 1:1 alpha G > 2:1 alpha G > 1:1 beta T or 2:1 alpha T. The preference for the alpha G type was also confirmed by investigating the host frameworks of the crystals obtained from binary mixtures. The dependence of the selectivity on the different types of CA crystals can be understood in terms of the fit of the guest molecule in the host cavity.

Benzene↗
PubMed1981

Thin-layer chromatographic separation of conjugates of ursodeoxycholic acid from those of litho-, chenodeoxy-, deoxy-, and cholic acids.

Separation of the glycine and taurine conjugates of ursodeoxycholic acid from those of lithocholic acid, chenodeoxycholic acid, deoxycholic acid, and cholic acid by thin-layer chromatography is described. Thus, on running a silica gel G plate first in a solvent system of n-butanol-water 20:3 and then in a second solvent system of chloroform-isopropanol-acetic acid-water 30:20:4:1, all the above-mentioned conjugated bile acids are separated from one another. The application of this method to study the change in the biliary bile acid conjugation pattern in ursodeoxycholic acid-fed gallstone patients is described.

Chenodeoxycholic Acid↗
PubMed1994

Resistance of aberrant crypt foci to apoptosis induced by azoxymethane in rats chronically fed cholic acid.

We have previously shown that chronic feeding of cholic acid to carcinogen treated rats reduces the number of putative preneoplastic lesions of colonic cancer, aberrant crypt foci (ACF), but enhances the growth of remaining ACF and the incidence of colonic tumors. The following study was conducted to further explore the effects of cholic acid on ACF growth by determining if ACF in cholic acid-fed animals display resistance to apoptotic cell death. ACF were induced in male Sprague-Dawley rats with two injections of azoxymethane (20 mg/kg body wt). Rats were divided into two groups and fed either the control AIN-76 diet or the AIN-76 diet containing 0.2% cholic acid. After 18 weeks, colonic apoptotic cell death was induced with an acute low dose of azoxymethane (10 mg/kg body wt). The number of cells, apoptotic bodies and bromodeoxyuridine (BUdR)-labeled cells were determined in colonic crypts comprising ACF and surrounding normal crypts in rats from each diet group. The number of apoptotic bodies per 100 cells was lower in ACF crypts than in normal-appearing crypts (P = 0.0034). Both normal and ACF crypts from rats fed the cholic acid diet had fewer apoptotic bodies per 100 cells than crypts from rats fed the control diet (P = 0.0102). These data suggest that ACF harbor resistance to induction of apoptosis. Chronic feeding of a diet containing 0.2% cholic acid results in the development of increased resistance to apoptosis. The lower rate of cell death in ACF may contribute to the enhanced growth of ACF and higher tumor incidence previously observed in cholic acid-fed animals.

Animals↗
PubMed1992

Formation of cholic acid from 3 alpha, 7 alpha, 12 alpha-trihydroxy-5 beta-cholestanoic acid in human skin fibroblasts.

Whether 3 alpha, 7 alpha, 12 alpha-trihydroxy-5 beta-cholestanoic acid (THCA) was converted into cholic acid in human skin fibroblasts was examined. THCA was incubated with subcellular fractions of cultured skin fibroblasts in the presence of NAD+, ATP, CoA, and Mg2+. The reaction products were analyzed by thin-layer chromatography and high-performance liquid chromatography after p-bromophenacyl ester derivatization. The highest specific activity was found in the light mitochondrial fraction (2.71 nmol/mg protein/h). The specific activity was about 9-fold higher than that in heavy mitochondrial fraction. The peroxisomal fraction prepared from the light mitochondrial fraction by sucrose gradient centrifugation was also able to catalyze the conversion of THCA into cholic acid. The specific activity in this fraction was a further 2.2-fold higher than that in the light mitochondrial fraction. These results suggest that cultured human skin fibroblasts are able to convert THCA into cholic acid, and that the activity exists in peroxisomes.

Catalase↗
PubMed1978

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

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

Alkaline Phosphatase↗
PubMed1986

Effects of cholic acid infusion in fetal lambs.

The effects of prolonged intravenous infusions of cholic acid into fetal lambs are described in this study. The ewes (n = 10, 11 fetuses) were operated on at 114 days of gestation (term = 150 days) by placing plastic catheters in maternal and fetal vessels and in the amniotic cavity. Gestational ages were confirmed after delivery by radiographic examination of the ossification centers of the fetal legs. Infusions of cholic acid (1.6 mumoles/min-1) started 8 to 10 days after surgery in 5 fetuses (including one twin). The remaining 6 fetuses (also including one twin) were infused with 5% dextrose in water. Total plasma bile acids at the beginning of the experiment were similar in both groups (23.8 +/- 6.6 vs. 24.3 +/- 5.7 microM). No significant changes in fetal heart rate, blood pressure, blood gases or pH were detected during the infusion. Meconium-stained amniotic fluid was observed during the third day of infusion in all the fetuses infused with cholic acid and in one control fetus. Fetuses infused with cholic acid were delivered alive 19-26 days before term. The concentration of plasma bile acids in the experimental group at delivery was 829 +/- 305 microM, i.e. significantly higher than that of the control group (24.4 +/- 5.7 microM). Control fetuses (except one twin) were delivered at term. We concluded that cholic acid, even at the high dose infused, is neither lethal nor severely harmful for the fetus. Meconium passage of the fetuses infused with cholic acid, in our experiment, appeared to be related to the stimulatory effect of cholic acid on fetal colonic motility rather than to fetal hypoxia.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1991

Mechanism of intestinal 7 alpha-dehydroxylation of cholic acid: evidence that allo-deoxycholic acid is an inducible side-product.

We previously reported that the 7 alpha-dehydroxylation of cholic acid appears to be carried out by a multi-step pathway in intestinal anaerobic bacteria both in vitro and in vivo. The pathway is hypothesized to involve an initial oxidation of the 3 alpha-hydroxy group and the introduction of a double bond at C4-C5 generating a 3-oxo-4-cholenoic bile acid intermediate. The loss of water generates a 3-oxo-4,6-choldienoic bile acid which is reduced (three steps) yielding deoxycholic acid. We synthesized, in radiolabel, the following putative bile acid intermediates of this pathway 7 alpha,12 alpha-dihydroxy-3-oxo-4-cholenoic acid, 7 alpha,12 alpha-dihydroxy-3-oxo-5 beta-cholanoic acid, 12 alpha-dihydroxy-3-oxo-4,6-choldienoic acid, and 12 alpha-hydroxy-3-oxo-4-cholenoic acid and showed that they could be converted to 3 alpha,12 alpha-dihydroxy-5 beta-cholanoic acid (deoxycholic acid) by whole cells or cell extracts of Eubacterium sp. VPI 12708. During studies of this pathway, we discovered the accumulation of two unidentified bile acid intermediates formed from cholic acid. These bile acids were purified by thin-layer chromatography and identified by gas-liquid chromatography-mass spectrometry as 12 alpha-hydroxy-3-oxo-5 alpha-cholanoic acid and 3 alpha,12 alpha-dihydroxy-5 alpha-cholanoic (allo-deoxycholic acid). Allo-deoxycholic acid was formed only in cell extracts prepared from bacteria induced by cholic acid, suggesting that their formation may be a branch of the cholic acid 7 alpha-dehydroxylation pathway in this bacterium.

Bile Acids and Salts↗
PubMed1981

Formation of urso- and ursodeoxy-cholic acids from primary bile acids by Clostridium absonum.

Eight strains of Clostridium absonum were shown to form ursocholic acid (UC) from cholic acid (C) and ursodeoxycholic acid (UDC) from chenodeoxycholic acid (CDC) but did not transform deoxycholic acid (DC) in whole cell cultures. The structures of UC and UDC were verified by mass spectroscopy, and by thin-layer chromatography using Komarowsky's spray reagent. The organism transformed C and CDC at concentrations below 1.5. 10(-3) M and 5.0. 10(-4) M, respectively; higher concentrations were inhibitory. Optimal yields of the final products were realized at about 15-22 hr and 9-15 hr of incubation, respectively, and were in the range of 60-70%. Additionally, the 7 keto-derivatives, 7 keto-deoxycholic acid (7K-DC) or 7 keto-lithocholic acid (7K-LC) were also formed from C and CDC. With longer periods of incubation, increasing yields of 7K-DC and 7K-LC and decreasing yields of UC and UDC were observed. These time course studies suggest that 7K-DC and 7K-LC are intermediates in the formation of UC and UDC from the primary bile acids. We propose the occurrence of C right harpoon over left harpoon 7K-DC right harpoon over left harpoon UC and CDC right harpoon over left harpoon 7K-LC right harpoon over left harpoon UDC with increasing dominance of back reaction of the second step on aging of the culture. When the initial pH value of the medium was manipulated within the range of 5.8-9.0, increasing yields of UDC from CDC were obtained at higher pH values (maximum yield at pH 9.0 was 83%), with total inhibition of growth and transformation at pH 5.8. In contrast, UC was produced from C at all pH values studied, with marginal differences in yields (maximum yield at pH 8.0 was 50%). In all cases, formation of UC from C was much slower than that of UDC from CDC. In contrast, C. paraperfringens transformed none of the above bile acids. We propose that C. absonum, or a biochemically similar species, may be present in the human gut and give rise to UDC (and UC) in vivo.-Macdonald, I. A., D. M. Hutchison, and T. P. Forrest. Formation of urso- and ursodeoxycholic acids from primary acids by Clostridium absonum.

Bile Acids and Salts↗