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At least 19 recordsLinked to original sources
PubMed2006

Regio- and stereoselective reductions of dehydrocholic acid.

Dehydrocholic acid (DHCA), an unnatural bile acid, is manufactured by oxidation of cholic acid. Its biotransformation by two basidiomycetes (Trametes hirsuta and Collybia velutipes) is reported. These mycelia showed different affinities for the substrate and selectivities of attack: T. hirsuta in particular regio- and stereoselectively reduced the 3-keto group to yield 3 alpha-hydroxy-7,12-diketo-5 beta-cholan-24-oic acid (7,12-diketolithocolic acid) as the main product. A number of different chemical reductions were carried out on DHCA; among them hydrogenation with Raney Nickel in water under high-intensity ultrasound proved highly regio- and stereoselective, yielding 7,12-diketolithocolic acid exclusively. (1)H and (13)C resonances were assigned in details thanks to a series of 1D and 2D NMR runs including DEPT, NOESY, H-H COSY, gHSQC and gHMBC.

Basidiomycota↗
PubMed1987

Enzymes involved in the formation of 3 beta, 7 beta-dihydroxy-12-oxo-5 beta-cholanic acid from dehydrocholic acid by Ruminococcus sp. obtained from human intestine.

Ruminococcus sp. PO1-3 from human intestinal flora reduced dehydrocholic acid to 3 beta-hydroxy-7,12-dioxo-5 beta-cholanic acid by means of the enzyme 3 beta-hydroxysteroid dehydrogenase (Akao, T., Akao, T., Hattori, M., Namba, T. and Kobashi, K. (1986) J. Biochem. (Tokyo) 99, 1425-1431). This bacterium and its crude extract gave rise to another product, showing a lower RF value on TLC, from dehydrocholic acid. The product was identified as 3 beta, 7 beta-dihydroxy-12-oxo-5 beta-cholanic acid. The crude extract reduced 7-ketolithocholic acid and its methyl ester, but not 6-ketolithocholic acid and 12-ketochenodeoxycholic acid, in the presence of NADPH, and oxidized ursodeoxycholic acid and beta-muricholic acid, but not cholic acid, chenodeoxycholic acid, deoxycholic acid and hydrocholic acid, in the presence of NADP+. Therefore, besides 3 beta-hydroxysteroid dehydrogenase, 7 beta-hydroxysteroid dehydrogenase was shown to be present in this bacterium. The two dehydrogenases were clearly separated from each other by butyl-Toyopearl 650 M column chromatography. From dehydrocholic acid, 7 beta-hydroxy-3,12-dioxo-5 beta-cholanic acid was produced by 7 beta-hydroxysteroid dehydrogenase and 3 beta, 7 beta-dihydroxy-12-oxo-5 beta-cholanic acid was produced by combination of two enzymes, 7 beta- and 3 beta-hydroxysteroid dehydrogenase.

3-Hydroxysteroid Dehydrogenases↗
PubMed1976

The influence of cholic acid and dehydrocholic acid on the biliary excretion of unconjugated and conjugated sulfobromophthalein in rats.

Urethane anesthetized Wistar rats with biliary fistulas were infused during 100 min with sulfobromophthalein (BSP), the glutathione conjugate of sulfobromophthalein (BSP-GSH), cholic acid (CA) and dehydrocholic acid (DCA). The dyes (594 nmol/100 g/min) and the bile acids (1200 nmol/100 g/min) were infused separately, and in combination as well. When BSP was infused, CA and DCA increased the maximal excretion of total BSP (conjugated plus unconjugated) from 1400 to 4100 and 3300 nmol/100 g/10 min. The bile flow observed with BSP plus CA was not significantly different from that with BSP plus DCA. The biliary excretion of total BSP was higher throughout with CA than with DCA because CA increased the biliary concentration of PSP while DCA did not. The bile flow attained with CA alone was significantly lower than that with BSP plus CA. The current data provide arguments for abandoning the view that choleresis per se is the crucial determinant for BSP excretion. When BSP-GSH was infused instead of BSP, the excretion rate of the dye was not altered by the additional infusion of CA whereas it was significantly reduced by DCA. The maximal biliary concentration of BSP-GSH fell from 25.9 nmol/mul to 15.3 and 9.4 nmol/mul with CA and DCA, respectively. Both CA and DCA impaired the hepatic uptake of BSP and BSP-GSH. During the infusion with CA, BSP plus CA and BSP-GSH plus CA the biliary excretion rates of bile acids did not differ significantly from each other. This favours the view that the transfer for CA from the liver to bile is different from that for BSP and BSP-GSH. A fraction of bile fluid "independent of choleretics" (viz. of bile salts, BSP and BSP-GSH) is estimated and discussed in view of the different types of infusion.

Animals↗
PubMed1976

[Effect of ursodeoxycholic acid on bile secretion and bile components. Comparison with chenodeoxycholic acid and dehydrocholic acid].

Effects of some bile acids on the biliary flow, BSP output and composition (phospholipid, cholesterol, bilirubin and bile acids) were studied in dogs. Ursodeoxycholic acid (UD), chenodeoxycholic acid (CD) and dehydrocholic acid (DC) caused a dramatic increase in biliary flow and BSP output. Relative potencies of these effects were DC greater than CD greater than or equal to UD. UD increased the phospholipid, bile acids and cholesterol concentration but had little effect on bilirubin concentration. Furthermore, UD greatly increased the output of four bile components. CD slightly decreased the phospholipid, cholesterol and bilirubin concentration without the bile acids, while CD increased the output of bile components. After UD or CD administration, the bile acid of each appeared markedly in the bile, dose dependently. On the other hand, DC caused a dramatic decrease of phospholipid, cholesterol and bilirubin concentration but had little effect on bile acids concentration. Output of bile components was increased by DC the first 1 hr but decreased at 2 hr. After DC administration, 3alpha, 7alpha-dihydroxy-12keto-5beta-cholanic acid appeared in the bile while DC did not. Therefore, it is concluded that UD and CD are cholanereticas and DC is a hydrocholeretica.

Animals↗
PubMed1980

[Choleretica properties of chenodeoxycholic acid CDCA and dehydrocholic acid (DHCA) in rats (author's transl)].

Mechanisms of hepatic bile secretion were studied in unanesthetized bile fistula rats. After implantation of bile fistula, bile flow and bile acids secretion were significantly decreased and secondary bile acids were greatly decreased. After cholic acid (CA) 30 microM/100 g/hr infusion, bile juice was greatly increased, and CA was dramatically increased in bile. Biliary bile flow and bile acid were not increased after infusion of CDCA 30 microM/100 g/hr. CDCA was slightly increased in bile, but the amount of bile acids tended to decrease. DHCA dramatically increased the amount of bile juice, while DHCA was not detected in the bile. After DHCA infusion, 3 alpha, 7 alpha-dihydroxy-12-keto-5 beta-cholanic acid dramatically increased and slightly increased in CA. Regarding the relationship between the bile flow rate and the secretion rate of the total bile acids, bile acid-dependent bile secretion varied with the bile acid value. On the other hand, Na+ and K+ concentrations of bile were not related to bile acid concentration. These studies show that canalicular bile secretion mechanisms varied with the compositions of bile acids and bile acid secretion rate.

Animals↗
PubMed1989

The biotransformed metabolite profiles in blood after intravenous administration of dehydrocholic acid.

One gram of dehydrocholic acid was injected intravenously into two patients with percutaneous transhepatic cholangial drainage, and the biotransformed metabolites profiles over a 120-min period in serum and bile were analyzed. In serum unconjugated 3 alpha-hydroxy-7,12-dioxo-cholanoic acid (3 alpha-OH-7,12-OXO) acid was markedly increased after the injection of dehydrocholic acid, and reached about 80 microM within 30 min. On the other hand, conjugated 3 alpha, 7 alpha-dihydroxy-12-oxo-cholanoic acid (3 alpha,7 alpha-OH-12-OXO) was consecutively increased with lag time to an elevation of 3 alpha-OH-7,12-OXO. In bile, the major constituent of metabolites was conjugated 3 alpha,7 alpha-OH-12-OXO (more than 90% of the excreted metabolites), while conjugated 3 alpha-OH-7,12-OXO was detected as minor constituent. Therefore, between bile and serum, there was great difference in biotransformed metabolites profiles. The mechanism of elevation of unconjugated 3 alpha-OH-7,12-OXO in serum remains obscure, but this new finding raised a question as to whether organ-reducing 3-keto group of dehydrocholic acid is restricted to the liver.

Aged↗
PubMed1993

[Effects of dehydrocholic acid (Biliton) on metabolism and liver function in cows].

Dehydrocholic acid (Biliton) was given to 9 cows with a predisposition for the fat mobilization syndrome in daily doses of 5.5 g each. This was done two weeks after parturition and the results were compared with those from 9 untreated cows. Five other cows suffering from ketosis or indigestion symptoms were treated too. Decreased concentrations of liver lipids, free fatty acids (FFA), bilirubin, beta-OH-butyrate and urea as well as increased glucose in blood plasma indicated a favourable action of Dehydrocholic acid on metabolism and liver function. We did not observe a significant influence on milk and reproduction parameters. The use of Dehydrocholic acid is recommended for use in liver disturbances.

Animals↗
PubMed1973

Triketocholanoic (dehydrocholic) acid. Hepatic metabolism and effect on bile flow and biliary lipid secretion in man.

[24-(14)C]Dehydrocholic acid (triketo-5-beta-cholanoic acid) was synthesized from [24-(14)C]cholic acid, mixed with 200 mg of carrier, and administered intravenously to two patients with indwelling T tubes designed to permit bile sampling without interruption of the enterohepatic circulation. More than 80% of infused radioactivity was excreted rapidly in bile as glycine- and taurine-conjugated bile acids. Radioactive products were identified, after deconjugation, as partially or completely reduced derivatives of dehydrocholic acid. By mass spectrometry, as well as chromatography, the major metabolite (about 70%) was a dihydroxy monoketo bile acid (3alpha,7alpha-dihydroxy-12-keto-5beta-cholanoic acid); a second metabolite (about 20%) was a monohydroxy diketo acid (3alpha-hydroxy-7,12-di-keto-5beta-cholanoic acid); and about 10% of radioactivity was present as cholic acid. Reduction appeared to have been sequential (3 position, then 7 position, and then 12 position) and stereospecific (only alpha epimers were recovered). Bile flow, expressed as the ratio of bile flow to bile acid excretion, was increased after dehydrocholic acid administration. It was speculated that the hydroxy keto metabolites are hydrocholeretics. The proportion of cholesterol to lecithin and bile acids did not change significantly after dehydrocholic acid administration. In vitro studies showed that the hydroxy keto metabolites dispersed lecithin poorly compared to cholate; however, mixtures of cholate and either metabolite had dispersant properties similar to those of cholate alone, provided the ratio of metabolite to cholate remained below a value characteristic for each metabolite. These experiments disclose a new metabolic pathway in man, provide further insight into the hydrocholeresis induced by keto bile acids, and indicate the striking change in pharmacologic and physical properties caused by replacement of hydroxyl by a keto substituent in the bile acid molecule.

Bile↗
PubMed1990

Influence of dehydrocholic acid on the secretion of bile acids and biliary lipids in rats.

This study investigated the influence of dehydrocholic acid (DHCA) infusion on the secretion of endogenous bile acids, and biliary lipids in rats in an attempt to explain the reduction of biliary lipid secretion associated with DHCA infusion. DHCA increased bile flow and the bile acids produced during the infusion were composed of three hydroxy-oxo metabolites (83-93%), and cholic acid (6-14%). Very little DHCA was secreted unchanged (less than 2%). The secretions of all the endogenous biliary bile acids were diminished within 30-60 min of infusion. DHCA furthermore reduced the secretion of exogenous cholic acid when co-infused with DHCA. Phospholipid secretion declined to an undetectable amount and cholesterol declined to 10% of the base value by the end of the infusion. The reduction of biliary lipid secretion during DHCA infusion was attributed to the diminished secretion of endogenous bile acids. These data show that DHCA infusion induces choleresis associated with reduced secretion of endogenous and/or exogenous biliary components.

Animals↗
PubMedDate not supplied

[Chronopharmacological characteristics of the action of dehydrocholic acid on bile formation].

Peculiarities of the liver response to dehydrocholic acid, conditioned by the time of its administration during the day and by the seasons of the year were revealed in experiments on random bred mature white rats. The dependence of this reaction on the time factor was manifested in all the main indicators of cholopoiesis--in the rate of bile secretion, synthesis and secretion of bile acids and bilirubin, cholesterol excretion.

Animals↗
PubMed1990

Studies on the origin of biliary phospholipid. Effect of dehydrocholic acid and cholic acid infusions on hepatic and biliary phospholipids.

The correlation between the secretion of biliary phospholipid (PL) and bile acid suggests a regulatory effect of bile acid on PL secretion. Bile acids may influence PL synthesis and/or the mobilization of a preformed PL pool. The objective of this study was to determine the contribution of these two sources to biliary PL, by using an experimental protocol in which dehydrocholic acid (DHCA) and cholic acid (CA) were infused to manipulate biliary PL secretion. In control rats, there was a steady state in bile flow. PL secretion and the biliary secretion of newly synthesized phosphatidylcholine (PC). The specific radioactivity of PC in bile was significantly higher than in plasma, microsomes and canalicular membranes. DHCA infusion decreased biliary PC secretion rate by 80%, and secretion returned to normal values at the transport maximum of CA. The specific radioactivity of biliary PC was decreased by 30% by DHCA infusion and reached normal values during CA infusion. There were no significant changes in the specific radioactivity of PC in plasma or cellular organelles during infusion of bile acids. These data indicate that: (1) newly synthesized PC contributes a small percentage to biliary PC; thus a preformed pool (microsomal and extrahepatic) is a major source of biliary PL; (2) the contribution of the extrahepatic pool to the biliary PL may be more important than the microsomal pool.

Animals↗
PubMed1973

Alterations in biliary lipids of mice during dehydrocholic acid feeding.

Mice were fed a lithogenic diet consisting of Purina chow and 0.5% dehydrocholic acid (DHA group). Controls received Purina chow. Every 2 wk for 20 wk animals were killed, and biliary phospholipid, cholesterol, and bile salt concentrations were determined, as well as the extent of gallstone formation. With time there was a gradual, significant decline in the concentration and the relative composition of phospholipid in both groups compared with initial values. There was a significant increase in biliary cholesterol concentration and relative amount in the DHA group compared with the control. No significant differences were found in the relative amounts of bile salt or phospholipid between the two groups. Feeding DHA resulted in an increased concentration of bile salts and the sum of measured lipid compared with controls. After 8 wk, gallstones were found in approximately 60% of autopsied animals and correlated with increased cholesterol concentration. Our data support the hypothesis that there is a component of cholesterol secretion that may not be bile salt- or phospholipid-dependent. Our data also suggest that biliary phospholipid secretion decreases with age.

Administration, Oral↗