SEARCH · PubMed Health

Results for “CHOLIC ACID”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 127 records · Page 7Linked to original sources

PubMed1976

Equilibrium-dialysis studies of the interaction between cholic acid and 100000g-supernatant preparations from the rat liver.

1. The binding of cholic acid to 100000g supernatants from rat livers was investigated by equilibrium dialysis and gel-exculsion chromatography. 2. Supernatants were found to contain at least two classes of binding site for cholic acid. 3. These recptor molecules are probably proteins since incubation with proteolytic enzymes resulted in complete loss of cholic acid binding. 4. Supernatants were added to columns of Sephadex G-75, and two groups of fractions were shown to bind cholic acid. One of these contained low-affinity binding sites and the other contained both low- and high-affinity binding sites. 5. Feeding cholestyramine had no effect on cholic acid binding. 6. Increased cholic acid binding occurred after injection of phenobarbitone. There was an increase in the amount of the low-affinity component but no change in the high-affinity component. 7. The dissociation constants of the binding of cholic acid suggest that the binding proteins may be involved in bile acid transport.

Animals↗

PubMed1985

Acute effects of dietary cholic acid and methylazoxymethanol acetate on colon epithelial cell proliferation; metabolism of bile salts and neutral sterols in conventional and germfree SD rats.

The acute effects of cholic acid ingestion on methylazoxymethanol acetate [(MAM) CAS: 592-62-1]-treated conventional and germfree rats were investigated. Male SD rats were divided into 4 treatment groups. The first group received control chow; the second group, control chow plus 0.5% cholic acid; the third group, control chow plus MAM; and the fourth group, control chow plus 0.5% cholic acid plus MAM. Fecal bile acids, cholesterol, cholesteral degradation products, and neutral sterols, as well as labeling indices and numbers of epithelial cells per crypt column, were measured after 6 weeks of treatment. The administration of MAM to germfree groups diminished both fecal bulk and the amount of fecal water. MAM did not affect the fecal bile acid composition. Analysis of the fecal bile acids in conventional rats fed cholic acid demonstrated that half of the bile acids were in a form of deoxycholic acid. In the germfree groups fed cholic acid, 90% of the bile acids appeared unaltered in the feces. Neither in the germfree nor in the conventional groups was an effect seen of MAM on the output of fecal neutral sterols. The addition of cholic acid to the food decreased the output of neutral sterols both in the conventional (P less than .001) and in the germfree (P less than .02) animals. The germfree animals showed a reduced amount of neutral steroid excretion (P less than .01) when compared to the findings for the conventional groups. MAM had no influence on the fecal cholesterol or coprostanol output. The consumption of 0.5% cholic acid decreased the total output of cholesterol (P less than .05). The excretion of coprostanol was significantly diminished in the conventional rats fed cholic acid (P less than .001). No difference in labeling indices was observed between conventional and germfree rats, whether treated with cholic acid, MAM, or cholic acid plus MAM. However, all germfree groups showed less epithelial cells per crypt column (P less than .001) than did conventional animals.

Animals↗

PubMed1997

Induction of sodium-dependent bile acid transporter messenger RNA, protein, and activity in rat ileum by cholic acid.

BACKGROUND & AIMS: The ileal sodium-dependent bile acid transporter reclaims bile acids from the intestinal lumen to preserve their enterohepatic recirculation. The present studies sought to determine the possible role of enteric bile acids in the molecular regulation of the apical bile acid transporter in rat ileal mucosa. METHODS: Paired rats were fed a control diet or control diet plus cholic acid (1%) or ursodeoxycholic acid (1%) for 10 days. Other paired rats underwent biliary diversion for 72 hours, followed by intraduodenal infusion of taurocholate or fluid/electrolytes. Transporter protein, messenger RNA (mRNA), and activity were determined in the distal 15 cm of ileal mucosa. RESULTS: Transporter protein and mRNA levels in cholic acid-fed rats increased approximately threefold above levels in paired rats fed the control diet (P < 0.02). Similarly, sodium-dependent [3H]taurocholate uptake into membrane vesicles from cholic acid-fed rats increased twofold above uptake into vesicles from control-fed rats because of a twofold increase in maximal transport velocity. In biliary-diverted rats (72-96 hours), transporter protein decreased to 57% +/- 5% of paired controls with intact enterohepatic circulation (P < 0.0001). The intraduodenal infusion of taurocholate (24 hours) in biliary-diverted rats resulted in a time-dependent reinduction of transporter protein expression (3.5-fold). CONCLUSIONS: The expression of the ileal apical bile acid transporter is induced at a pretranslational level by free or taurine-conjugated cholic acid within the small intestine.

Animals↗

PubMed1985

Influence of age, dietary cholic acid, and calcium levels on performance, utilization of free fatty acids, and bone mineralization in broilers.

The effects of age on the utilization of dietary palmitic or a 50/50 mixture of palmitic and oleic acid at the 8% inclusion level in the absence or presence of .2% cholic acid and also in the presence of low (.8%) or high (1.2%) calcium were investigated using broiler chicks from 1 to 56 days of age. Significant interactions (P less than .01) were observed between the type of fatty acid supplemented and the presence or absence of cholic acid on weight gain and feed efficiency. Supplementing diets with a mixture of equal weights of palmitic and oleic acid, reduced feed intake relative to control diets and diets supplemented with palmitic acid alone. There was an interaction between the age of the bird and the type of fatty acid supplemented on fat retention and metabolizable energy (ME) of diets (P less than .01). There was also a significant interaction between the type of fatty acid supplemented and the addition of cholic acid on fat retention and ME of diets. While cholic acid reduced soap formation during the process of digestion (P less than .05), increasing dietary calcium level increased the proportion of the digesta fat that was present as soap (P less than .01). The proportion of digesta and excreta fat, present as soap, depended on the type of fatty acid supplemented. The addition of free fatty acids to broiler diets resulted in a decrease in bone ash and bone calcium content relative to those birds fed the control diet. It is concluded that the ability of broilers to utilize dietary free fatty acids depends on the age at which they are fed, although in all cases supplemental cholic acid enhances fatty acid utilization.

Aging↗

PubMed1979

Formation of cholic acid via 3 alpha, 7 alpha,12 alpha-trihydroxy-5 beta-cholestan-26-oic acid in the dog.

The proposed cholic precursor, 3 alpha, 7 alpha, 12 alpha-trihydroxy-5 beta-[3H]cholestan-26-oic acid, and [14C]cholesterol were infused intravenously at a constant rate into two dogs for 25 days. If the specific activities of trihydroxy[3H]cholestanoic acid and [3H]cholic acid will be equal after an isotopic steady-state is achieved. The specific activities of [14C]deoxycholic acid (formed from [14C]cholic acid) isolated in the stool of these two dogs were equal the last four days of the infusion indicating that labeled deoxycholic acid (and presumably labeled cholic acid) was in an isotopic steady-state. However, the specific activities of trihydroxy[3H]cholestanoic acid were 3.3 and 5.7 times greater than the specific activities of [3H]cholic acid, respectively. These data suggest that either an alternate route of cholic acid synthesis exists exclusive of trihydroxycholestanoic acid or that an isotopic steady state of trihydroxycholestanoic acid cannot be reached during an infusion of labeled trihydroxycholestanoic acid.

Animals↗

PubMed1991

Abnormal low ratio of cholic acid to chenodeoxycholic acid in a cholestatic infant with severe hypoglycemia.

We report a premature infant with severe hypoglycemia (serum glucose: 6 mg/dl) and cholestasis (serum total bile acids: 211.55 mumol/L) caused by hypoplasia of the interlobular bile ducts. This patient had developed intracranial hemorrhage and sepsis while undergoing treatment for hypoglycemia. As a result of endocrine evaluation, we made a diagnosis of idiopathic panhypopituitarism, congenital absence or hypoplasia of the pituitary gland. Moreover, we found abnormal bile acid profiles: The ratio of cholic acid to chenodeoxycholic acid was abnormally low in serum (0.04) and in biliary bile (0.33). However, 3 alpha,7 alpha,12 alpha-trihydroxy-5 beta-cholestan-26-oic acid and bile alcohols were not detected. We therefore suspected that the severe cholestasis and abnormal bile acid profiles in the serum and biliary bile in this patient were related to physiologic immaturity of the enterohepatic circulation of bile acids and immaturity of hepatic 12 alpha-hydroxylation.

Adult↗

PubMed1987

Metabolism of the bile acid analogues 7 beta-methyl-cholic acid and 7 alpha-methyl-ursocholic acid.

The metabolism of two new bile acid analogues, 7 beta-methyl-cholate and 7 alpha-methyl-ursocholate, was compared with that of cholate in the hamster. After intraduodenal administration of 14C-labeled compounds into bile fistula hamsters, radioactivity was exclusively recovered in bile; the more hydrophobic bile acid was absorbed more rapidly. Hepatic extraction of intravenously infused compounds was efficient and administered analogues became major biliary bile acids. Amidation of cholate was essentially complete, whereas 39% of 7 beta-methyl-cholate and 65% of 7 alpha-methyl-ursocholate were secreted in unconjugated form. After intragastric administration of the compounds, radioactivity was quantitatively recovered in feces. Cholate was 7-dehydroxylated to deoxycholate, whereas 31% of 7 beta-methyl-cholate and 78% of 7 alpha-methyl-ursocholate were recovered unchanged. Fifty percent of 7 beta-methyl-cholate and 15% of 7 alpha-methyl-ursocholate were transformed into ketonic derivatives, without loss of the 7-hydroxyl group. It is concluded that the introduction of the 7-methyl group did not interfere with intestinal absorption, hepatic extraction, and biliary secretion but did affect enzymatic amidation and bacterial 7-dehydroxylation of the analogues.

Animals↗

PubMed1984

Formation of urso- and ursodeoxy-cholic acids from primary bile acids by a Clostridium limosum soil isolate.

A gram-positive, rod-shaped anaerobe (isolate F-14) was isolated from soil. This organism was identified by cellular morphology as well as by fermentative and biochemical data as Clostridium limosum. Isolate F-14 formed ursocholic acid (UC) and 7-ketodeoxycholic acid (7-KDC) from cholic acid (CA), and ursodeoxycholic acid (UDC) and 7-ketolithocholic acid (7-KLC) from chenodeoxycholic acid (CDC) in whole cell cultures, but did not transform deoxycholic acid (DC). No hydrolysis or transformation occurred when either taurine- or glycine-conjugated bile acids were incubated with F-14. The type stain of Clostridium limosum (American Type Culture Collection 25620) did not transform bile acids. The structures of ursocholic, ursodeoxycholic, 7-ketodeoxycholic, and 7-ketolithocholic acids were verified by mass spectroscopy and by thin-layer chromatography using Komarowsky's spray reagent. The organism transformed cholic and chenodeoxycholic acids at concentrations of 20 mM and 1 mM, respectively; higher concentrations of bile acids inhibited growth. Optimal yields of ursocholic and ursodeoxycholic acids were obtained at 9-24 hr of incubation and depended upon the substrate used. Increasing yields of 7-ketodeoxycholic and 7-ketolithocholic acids, and decreasing yields of ursocholic and ursodeoxycholic acids were observed with longer periods of incubation. Culture pH changed with time and was characterized by a small initial drop (0.2-0.4 pH units) and a subsequent increase to a pH (8.1-8.2) that was above the starting pH (7.4).(ABSTRACT TRUNCATED AT 250 WORDS)

Bile Acids and Salts↗

PubMed1989

Serum concentrations of unconjugated and conjugated cholic acid in portal venous and systemic venous blood of fasting man.

The fasting concentrations of unconjugated and conjugated cholic acid were determined in the peripheral venous serum of 15 healthy subjects, eight patients with ileal resection and six patients with known bacterial overgrowth of the upper small intestine. In addition, the estimated hepatic uptake of unconjugated and conjugated cholic acid was determined in 15 gallstone patients undergoing cholecystectomy. A highly accurate and specific mass-fragmentographic technique with high sensitivity was used. The proportion of unconjugated cholic acid averaged 34% in the healthy subjects. The estimated fractional hepatic uptake of unconjugated cholic acid was lower than that of conjugated cholic acid, 71% and 87%, respectively (means). Patients with ileal resection had an increased proportion of unconjugated cholic acid in their peripheral venous serum, 49% (mean). The patients with bacterial overgrowth of the upper small intestine also displayed a high proportion of unconjugated cholic acid, 63% (mean). It is suggested that determination of the proportion of unconjugated cholic acid in peripheral venous blood may possibly be used for detection of bacterial contamination of the upper small intestine.

Adult↗

PubMed1979

Nuclear and cytosolic distribution of conjugated cholic acid and radiolabelled glycocholic acid in rat liver.

1. Normally fed and cholestyramine-treated rats were injected through the superior mesenteric vein with different amounts of radiolabelled glycoholic acid and the appearance of radioactivity in bile was measured. 2. In normally fed rats radioactivity appeared in bile within 30 s of injection and reached a maximum after 2 1/2 min; in the cholestyramine-treated animals the appearance of radioactivity was slower and less of the injected material was excreted into bile. 3. At 10 min after injection, livers were removed and the amounts of radioactive glycoholic acid and endogenous cholic acid conjugates in nuclei and cytosol were determined; most of the bile acid was found in the cytosol, only small amounts being found in nuclei. 4. Nuclear preparations from both normally fed and cholestyramine-fed rats were extracted with KCl (0.4 M) in an attempt to identify a putative bile acid receptor, but no such receptor was found. 5. Regulation of bile acid synthesis does not involve nuclear binding of bile acids.

Animals↗

PubMed1981

Acute and chronic effect of dietary cholic acid on colonic epithelial cell proliferation.

Administration of cholic acid (1.0% of the diet) to male Fisher rats for 3 days resulted in increased numbers of DNA synthesizing epithelial cells per colonic crypt column as compared to those found in either control or 0.2% cholic acid-fed rats. The middle third of the crypt was the area stimulated to contribute the additional proliferating cells. The maximum number of 3H-TdR-labeled cells was doubled by 24 h and migration had processed further up the colonic crypt of the 1% cholic acid-fed rats than the 0.2% cholic acid or control animals. Compared with cholic acid-deprived rats, long-term dietary intake of 0.2% cholic acid (26 weeks) was found to heighten the numbers of labeled cells per column and expand the proliferative compartment. The enhanced manifestation of colonic neoplasia in MNU-induced rats consuming cholic acid (previously reported by us) appears related to the elevated levels of cell proliferation brought about in response to the deleterious action of the bile acid on the mucosa. Increased numbers of epithelial cells undergoing DNA synthesis in cholic acid-treated animals would allow the earlier expression of malignant transformation in the large intestine.

Animal Feed↗

PubMed1988

Suppression of hepatic HMG-CoA reductase activity by beta-muricholic acid in mice fed a diet containing cholesterol and cholic acid.

A diet containing cholesterol and cholic acid (SID) is known to induce the formation of cholesterol fatty liver as well as cholesterol gallstones. The activity of HMG-CoA reductase, one of the key enzymes for cholesterol synthesis in the liver, is significantly lowered by addition of beta-muricholic acid to SID. The prevention of fatty liver formation by beta-muricholic acid was accompanied by the suppression of HMG-CoA reductase activity.

Animals↗

PubMed2003

Cholic acid as template for multivalent peptide assembly.

Cholic acid, an amphiphilic steroid containing several selectively addressable functionalities, was exploited as a rigid template for multivalent peptide assembly. Thus, cholic acid-based templates suitable for chemoselective peptide ligation were synthesized, in which maleimide or bromoacetyl moieties were selectively introduced at the 3alpha, 7alpha, 12alpha-positions of cholic acid with varied length of linkers. Three peptides were chosen and tested for the chemoselective ligation. These include the HIV-1 peptide inhibitor DP178, the universal T-helper epitope derived from tetanus toxoid (830-844), and the minimum epitope sequence of the HIV-neutralizing antibody 2F5. It was found that the maleimide-functionalized templates are highly efficient for the ligation of all the peptides, while bromoacetyl templates led to low yield of ligation. Circular dichroism (CD) spectroscopic studies of the multivalent peptides (10a and 11a) containing three strands of peptide DP178 indicate that the template-assembled peptides form three alpha-helix bundles with significantly enhanced alpha-helix contents than the single peptide. The results suggest that cholic acid is a valuable template for constructing alpha-helix bundles that may be useful as mimics of conformational epitopes for vaccine development.

Amino Acid Sequence↗

PubMed1979

Metabolism of 5 beta-cholestane-3 alpha, 7 alpha, 12 alpha, 26-tetrol and 5 beta-cholestane-3 alpha, 7 alpha, 12 alpha, 25-tetrol into cholic acid in normal human subjects.

Side chain oxidation and cleavage of precursors in cholic acid synthesis is thought to involve initial hydroxylation at either position 25 or 26 of the side chain. Therefore, the conversion of 5 beta-cholestane-3 alpha, 7 alpha, 12 alpha, 26-tetrol and 5 beta-cholestane-3 alpha, 7 alpha, 12 alpha, 25-tetrol into cholic acid was studied in normal subjects after single intravenous injections of these labeled alcohols. Eighty-six percent and 82% of 5 beta-cholestane, 3 alpha, 7 alpha, 12 alpha, 26-tetrol was converted into cholic acid in two subjects, respectively. However, only 14 and 16% of the injected 5 beta-cholestane-3 alpha, 7 alpha, 12 alpha, 25-tetrol was converted into cholic acid in two subjects, respectively. Thus, this study indicates that 5 beta-cholestane-3 alpha, 7 alpha, 12 alpha, 25-tetrol is an inefficient substrate for cholic acid biosynthesis in man and that the major route of cholic acid synthesis probably involves the 26-hydroxylated intermediate.

Carbon Radioisotopes↗

PubMed1982

Effect of deoxycholic, chenodeoxycholic, and cholic acids on intestinal absorption of cholesterol in humans.

The effect of administration of primary and secondary bile acids on absorption of cholesterol was investigated in 15 volunteers. Eight Caucasians with radiolucent gallstones were studied before and after administration of chenodeoxycholic acid (all eight) and cholic acid (eight before, six after treatment) for 3 months, and seven healthy subjects were studied before and five were studied after administration of deoxycholic acid for 6 weeks. The hourly absorption of [3H]cholesterol was measured for 24 hours in a 20-cm duodenal segment by use of an intestinal perfusion technique. Fasting serum cholesterol and triglyceride levels were also measured before and after administration of bile acid. In patients with gallstones, absorption of cholesterol in the duodenum, expressed as the mean (+/- SEM) percentage of [3H]cholesterol absorbed hourly for 24 hours, was not significantly different after administration of chenodeoxycholic (22.5 +/- 4.4%) or cholic (25.6 +/- 5.9%) acid when compared with the pretreatment value (21.1 +/- 4.3%). Moreover, administration of chenodeoxycholic and cholic acid did not affect serum lipid levels. In contrast, administration of deoxycholic acid to healthy volunteers suppressed [3H]cholesterol absorption (13.2 +/- 3.2%) compared with that of the pretreatment period (26.5 +/- 3.8%) and decreased serum cholesterol levels by 15%. Our results suggest that chenodeoxycholic acid decreases the concentration of cholesterol in bile and dissolves gallstones by a mechanism other than inhibition of absorption of cholesterol. The data also indicate that the hypocholesterolemic effect of deoxycholic acid is due to the inhibition of intestinal absorption of cholesterol.

Adult↗

PubMed1999

Effects of cholic acid on blood pressure and production of vascular aldosterone and corticosterone.

The aims of this study were to search for the role of cholic acid in the regulation blood pressure of humans and rats and to investigate the effects of cholic acid on the production of vascular aldosterone and corticosterone in rats. Levels of serum total bile acids were measured by an enzymic spectrophotometeric method in normal controls, patients with essential hypertension, and in Wistar and spontaneously hypertensive rats. Levels in essential hypertension (7.3+/-3.4 micromol/l, n = 88) were higher than those of normal subjects (4.9+/-3.3 micromol/l, n = 86), and levels in SHR (13.9+/-3.8 micromol/l, n = 11) were slightly increased, but not significantly different from Wistar rats (10.4+/-5.1 micromol/l, n = 12). Male Wistar rats received cholic acid 80 mg/kg/day, orally, for 30 days, and blood pressure was monitored by a pressure transducer. Systolic blood pressure increased in Wistar rats treated with cholic acid compared to control rats. Mesenteric artery perfusion ex vivo was performed, and pressor responses to norepinephrine were determined in Wistar rats. The pressor responses to norepinephrine in mesenteric arteries treated with cholic acid were significantly increased. The perfusate from the mesenteric arteries was collected and applied to a Sep-Pak C 18 cartridge column for reverse phase high performance liquid chromatography, and levels of both aldosterone and corticosterone were determined by radioimmunoassay. Levels of aldosterone were decreased but those of corticosterone increased in the perfusate from arteries treated with cholic acid. Reverse transcriptase polymerase chain reaction showed that cholic acid inhibited the expression of 11beta-HSD2 and CYP11B2 mRNA in mesenteric arteries. These results reveal that cholic acid is able to induce hypertension and provide evidence that cholic acid inhibits the transcription of both 11beta-HSD2 and CYP11B2 in vasculature, leading to lower aldosterone and higher corticosterone production in vessels and increased vasoconstrictor responses to norepinephrine.

11-beta-Hydroxysteroid Dehydrogenases↗

PubMed1975

Inhibition of serum alkaline phosphatase activity by phenylalanine and cholic acid.

Serum alkaline phosphatase activity was found to increase more markedly in patients with liver cirrhosis than in patients with peptic ulcer and this increase was found to be influenced by blood types. After testing several amino acids and bile acids, phenylalanine and cholic acid were chosen and their inhibitory effects upon serum alkaline phosphatase activity were studied in 66 patients with various liver diseases. It was found that the combination of both agents demonstrates different patterns of inhibition between the patients with liver cirrhosis and obstructive jaundice. This inhibitory effects were also variable among cases of different blood types. Basing upon the present observation, the possible source of the elevated alkaline phosphatase activity in liver cirrhosis was discussed.

Alkaline Phosphatase↗

PubMed1993

Transformation of cholic acid by Arthrobacter simplex.

Fermentation of cholic acid with Arthrobacter simplex (IICB 227) under aerobic conditions yielded 3,12-dioxo-23,24-dinorchola-4,6-dienoic acid, 7 alpha-hydroxy-3,12-dioxo-23,24-dinorchol-4-enoic acid, 3 alpha, 7 alpha-dihydroxy-12-oxo-5 beta-cholan-24-oic acid, 3 alpha, 7 alpha-dihydroxy-12-oxo-5 beta-23,24-dinorcholan-22-oic acid, 7 alpha, 12 alpha-dihydroxy-3-oxo-5 beta-cholan-24-oic acid, 7 alpha-12 alpha-dihydroxy-3-oxo-4-cholenoic acid, 7 alpha, 12 alpha-dihydroxy-3-oxo-23,24-dinorchol-4-enoic acid, and methyl-3 alpha-7 alpha, 12 alpha-trihydroxy-5 beta-cholan-24-oate in addition to a new metabolite 2 beta-hydroxy-3,12-dioxo-23,24-dinorchola-4,6-dienoic acid. Each microbial metabolite was characterized by the application of various spectroscopic methods. The availability of some of the metabolites' enabled complete elucidation of their 13C NMR spectra.

Aerobiosis↗