SEARCH · PubMed Health

Results for “Taurocholic 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 19 recordsLinked to original sources

PubMed1977

The effect of para-aminobenzoic acid and taurocholic acid feeding on human bile composition.

Seven patients were investigated after cholecystectomy and exploration of the common bile duct to determine bile composition and excretion rates. An initial depression of the major components of bile stabilized by the sixth postoperative day. Feeding of para-aminobenzoic acid and taurocholic acid to these patients demonstrated an increase in excretion of total bile acids, taurine and glycine conjugates, cholates and deoxycholates. Para-aminobenzoic acid in the doses used failed to block glycine conjugation. Preferential conjugation of bile acid with glycine is due to a deficient taurine pool and not a preferential metabolic pathway.

4-Aminobenzoic Acid↗

PubMed1975

The effect of sodium benzoate and taurocholic acid feeding on human bile composition.

Four patients were fed sodium benzoate after stabilization following common bile duct exploration. Bile collections revealed no change in the output of glycine conjugated bile acids. Three patients had taurocholic acid added to the regimen after 3 days and demonstrated a significant increase in total and taurine conjugated bile acid output with marked reduction of the G/T ratio. These latter changes are similar to those produced by taurocholic acid feeding alone and therefore no benefit of the combination of drugs on bile salt excretion or conjugation ratio was demonstrated.

Benzoates↗

PubMed1978

The interaction of rifamycin SV with hepatic transport of taurocholic acid in the isolated perfused rat liver.

The effect of rifamycin SV on hepatic transport of taurocholic acid was investigated using isolated perfused rat liver technique. In all experiments, the perfused liver was maintained at taurocholic acid steady state by infusing constant amount of taurocholic acid. Infusion of rifamycin SV at various rates decreased biliary secretion of bile acids in a dose-dependent manner. Replacement of rifamycin SV by perfusion medium reversed this effect. To determine the site of action of rifamycin SV, kinetic experiments with 14C-taurocholic acid were undertaken. Rifamycin SV elevated the half-life of the medium disappearance of 14C-taurocholic acid. Furthermore, the antibiotic delayed the biliary appearance of 14C-taurocholic acid. The analysis of the results gave indications that the antibiotic interferred with hepatic uptake as well as biliary secretion of taurocholic acid.

Animals↗

PubMed1975

Role of taurocholic acid in production of gastric mucosal damage after ingestion of aspirin.

The possibility that aspirin-induced gastric mucosal damage may occur more readily in the presence of bile has been studied in man using measurement of transmucosal electrical potential difference as a marker of disruption of the gastric mucosal barrier. After the introduction of acetylsalicylic acid (600 mg) in suspension to seven subjects the mean electrical potential difference (plus or minus S.E. of mean) fell significantly from -33-3 plus or minus 2-0 mV to - 17-1 plus or minus 2-1 mV, and after the introduction of taurocholic acid (5 mmol/1) to seven other subjects the electrical potential difference fell significantly from -38-1 plus or minus 3-0 mV to-19-1 plus or minus 3-4 mV, the mean duration of these changes being 14-4 and 17-5 minutes respectively. When a combination of acetylsalicylic acid and taurocholic acid was introduced to eight subjects the mean electrical potential difference also fell significantly from -38-6 plus or minus 1-8 mV to -17-9 plus or minus 1-8 mV, but mean duration of this change (27 minutes) was significantly longer than that found after acetylsalicylic acid or taurocholic acid alone. These results indicate that the ingestion of aspirin, together with coincidental reflux of bile from duodenum, may be a factor in the pathogenesis of aspirin-induced gastric mucosal damage.

Aspirin↗

PubMed1975

Pepsin output after disruption of the human gastric mucosal barrier by taurocholic acid.

Test solutions containing 10 mM taurocholic acid in 160 mM HCl were instilled into the stomachs of healthy volunteers to disrupt the gastric mucosal barrier. Although significant back diffusion of hydrogen ions and exsorption of sodium ions occurred, there was no significant increase in pepsin output compared to control studies with 160 mm HCl alone. Our data suggest that 160 mM HCl produces a many-fold increase in basal pepsin output. In the innervated stomach of man disruption of the gastric mucosal barrier by taurocholic acid in acid solution is not accompanied by increased pepsin secretion compared to that produced by 160 mM HCl alone.

Adult↗

PubMedDate not supplied

Are non-absorbable indicators of comparable value in the human stomach made abnormal by taurocholic acid?

1. The substances chromium-51 (51CrCl3) and phenolsulphonphthalein (phenol red; PR) were compared as non-absorbable indicators in the human stomach after alteration of ionic permeability by taurocholic acid. 2. Control and test solutions containing 10 mM taurocholic acid and indicators at pH 1 were instilled into the stomach and sampled immediately and after 15 min. The ratios of the initial and final concentrations of the indicators (Ci/Cf) were compared. 3. Correlation coefficients of the Ci/Cf ratios for the two indicators were 0 with 91 in control studies and 0 with 75 after taurocholic acid instillation; there was no significant difference between either indicator. During taurocholic acid instillation, Ci/Cf values tended to fall compared to controls. 4. In a smaller number of subjects in whom polyethylene glycol (PEG) was also measured as a non-absorbable indicator, results were similar to those obtained with 51Cr and PR. 5. 51Cr, PR and PEG are comparable indicators in the normal human stomach and when it is made abnormal by a lipid-soluble agent such as unionized taurocholic acid, though the correlation between indicators is reduced in the abnormal stomach. 6. No evidence of increased absorption of any indicator was found in spite of the increased ionic permeability produced by taurocholic acid.

Absorption↗

PubMed1978

A compartmental model for hepatic transport of taurocholic acid in isolated perfused rat liver.

In order to characterize the transport of bile acids through the liver and to study the influence of drugs on these processes, a kinetic model for hepatobiliary transport of taurocholic acid (TC) using the isolated perfused liver was developed. After the system was brought to a steady state by infusing TC at a constant rate, a tracer dose of 14C-TC was injected into the medium. The medium disappearance of 14C-TC followed a first-order kinetic with a single rate constant. The plot of the biliary secretion rate of radioactivity versus time revealed a curve composed of at least three exponential components. From the described results and the present knowledge of hepatobiliary transport of bile acids we proposed a three compartment model, composed of a perfusion medium compartment and two liver compartments. Parameters calculated from the model constants agreed well with model-independent estimations. The influence of bromosulfophthalein (BSP) on the kinetic parameters was studied to compare the result with the known effect of BSP on hepatic transport of taurocholic acid. BSP decreased the constant describing the fractional transfer of taurocholic acid from medium into the liver, which is in agreement with the inhibition of hepatic uptake of taurocholic acid by BSP. Thus a three compartment model may adequately define the hepatobiliary transport of taurocholic acid in the isolated perfused rat liver.

Animals↗

PubMed1978

[Taurocholic acid synthesis in dogs maintained on a high cholesterol diet].

Labeled 35S-taurocholic acid synthesis was studied in dogs with gall bladder fistulae, fed high cholesterol diet. During the first period (1--2 months) dietary cholesterol caused a significant increase in the 35S-taurocholic acid synthesis. In 5--6 months, at the period of development of the pathological process in the liver, there was a decrease of synthesis and secretion of bile acids, and of cholesterol sediment in the bile. The level of plasma cholesterol in these dogs increased only slightly.

Animals↗

PubMed1979

Choleresis and cholestasis produced by infusion of taurocholic acid or taurodehydrocholic acid combined with BSP in the rhesus monkey.

To study the determinants of BSP Tm in rhesus monkeys, animals with indwelling silastic catheters were infused with sufficient BSP to produce a rising plasma concentration and normal saline or taurocholic acid 3.5 mumol/min, 7.0 mumol/min, or 10.5 mumol/min. BSP Tm was 3.84 +/- 0.11 mg/kg/10 min during normal saline infusion, 5.52 +/- 0.53 mg/kg/10 min during taurocholic acid 3.5 mumol/min, despite greater bile flow with the latter compound. Higher infusion rates of taurocholic acid inhibited BSP Tm and the proportion of conjugated BSP secreted into bile, as well as bile flow and bile acid secretion. Taurodehydrocholic acid 7.0 mumol/min produced similar but less marked effects. These results indicate that bile flow does not explain the effects of bile acids on BSP Tm and suggests that bile acids exert varying effects on BSP transport or binding in micelles. The cholestasis observed with combined BSP and higher bile acid infusion rates is probably due to inhibition of liver cell intermediary metabolism or to liver cell toxicity.

Animals↗

PubMed1979

Cholesterol metabolism in the liver and intestine of the chick: effect of dietary cholesterol, taurocholic acid and cholestyramine.

The effect of feeding cholesterol, taurocholic acid, or cholestyramine to chicks on cholesterogenesis from [1-14C] acetate in liver and intestine was determined in vitro using tissue slices, and in vivo by i.v. injection of [14C] acetate. The conversion of cholesterol to bile acids in liver in vivo was measured in the same treatments after i.v. injection of [3H] cholesterol. Hepatic cholesterogenesis in vitro and in vivo was depressed by dietary cholesterol and taurocholate and enhanced by cholestyramine. Intestinal cholesterogenesis in vivo was depressed only by taurocholate whereas ileal cholesterogenesis in vitro was reduced by dietary cholesterol. Conversion of cholesterol to bile acids was enhanced by dietary cholesterol and cholestyramine and depressed by taurocholate. Hepatic cholesterol metabolism in the chick appears to be regulated by mechanisms similar to those reported for other species.

Acetates↗

PubMed1977

The effect of the synthetic prostaglandin analog 15 (R) 15 methyl-PGE2 methyl ester on gastric mucosal hemorrhage induced in rats by taurocholic acid and hydrochloric acid.

The incidence of mucosal hemorrhage induced in rats by the oral administration of taurocholic acid (TCA) and hydrochloric acid (HCl) both singly and in combination was investigated. The effect of prostaglandin 15 (R) 15 methyl-PGE2 methyl ester (Me-PGE2) on the occurrence of hemorrhage induced by TCA with HCl was also studied. The incidence of hemorrhage induced by TCA (10 mM) alone and HCl (160 mM) alone was minimal and not different from that induced by the control solution. The combination of TCA (10 mM) and HCl (160 mM) produced bleeding in 67.7% of animals. The addition of 15 (R) 15 methyl-PGE2 methyl ester (9.9 micronM, corresponding to 50 microng/Kg) significantly reduced the incidence of hemorrhage induced by the combination of TCA with HCl from 67.7% to 31.3%. This suggests that this synthetic prostaglandin may be of value in conditions thought to be associated with reflux of bile into the stomach.

Animals↗

PubMedDate not supplied

The hepatic transport of taurocholic acid in the rat: development of a mathematical model.

1. The transport of taurocholic acid from portal blood to bile was studied in the anaesthetized rat by injecting a radiolabelled pulse of bile acid. 2. The transport process was very rapid, 50% of the dose being secreted within 5 min, and the total dose within 15 min. 3. The transport process had a large capacity. The secretory profile was little modified by a 500-fold increase in the injected dose. 4. The transport process was modelled with both analogue and digital computers. The simplest model which fitted the data comprised rapid uptake from portal blood, slow transport across the cell and rapid secretion into bile. The digital computer simulation suggested that this model is not unique, but will require further testing.

Animals↗

PubMed1975

Uptake of taurocholic acid into isolated rat-liver cells.

Binding and transport characteristics for uptake of taurocholic acid by isolated rat liver cells were studied. 1. An adsorption of taurocholate to the cell surface is terminated in less than 15 s. A Ks of 0.55 mM and a total binding capacity of 3.8 nmol/mg cell protein is determined. 2. The rate of uptake of taurocholate follows Michaelis-Menten kinetics with Km = 19 muM and V = 1.7 nmol/mg protein min. 3. There is a broad pH optimum for uptake between pH 6.5 -- 8.0. 4. The activation energy amounts to 29 kcal/mol. At high taurocholate concentration an unusual upward bend is observed in the Arrhenius plot. 5. Taurocholate uptake is competitively inhibited by taurochenodeoxycholate (Ki = 9 muM). It is noncompetitively inhibited by bromosulfophthalein (Ki = 3 muM). 6. At physiological taurocholate concentrations a 200-fold intracellular accumulation of taurocholate is observed. 7. Uptake is inhibited by about 75% by either antimycin A, carbonylcyanide m-chlorophenyl-hydrazone, ouabain. 8. Replacement of extracellular Na+ by either K+ or sucrose results in a 75% decrease of uptake. 9. It is concluded that taurocholate uptake is a carrier-mediated process, and suggested that the energy for intracellular accumulation is made available by cotransport of Na+.

Animals↗

PubMed1976

Effects of L-glutamine of acetylsalicylic acid or taurocholic acid-induced gastric lesions and secretory changes in pylorus-ligated rats under normal or stress conditions.

An oral dosing of either acetylsalicylic acid (ASA) or taurocholic acid (TCA) to pylorus-ligated rats subjected to water-immersion stress produced severe damage to the gastric musoca in contrast to the irritation observed in non-stressed ones. The irritative activity of ASA or TCA on gastric mucosa under stress was dose-dependent. Stress itself (23 degrees C, 7 hr) did not induce any appreciable changes in gastric mucosa under stress wasic mucosa of rats. L-glutamine, given together with SAS or TCA, significantly prevented the potentiated development of SAS- or TCA-induced gastric lesions in stressed rats. L-glutamine also prevented in varying degrees the reduction of acid and increment of Na+ ion in gastric juice accumulated in stressed rats in response to ASA or TCA.

Animals↗

PubMed1978