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Results for “DEHYDROCHOLIC ACID”

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PubMedDate not supplied

[A pharmacological analysis of liver secretory function under altered microsomal enzyme activity].

Inductors of the microsomal enzymes phenobarbital and, to a lesser extent, cordiamine stimulate the biligenic function of the liver, while the inhibitor monooxigenases cymetidine depresses it. Employment of bile-expelling agents, such as cholic and dehydrocholic acids, sodium selenate, under conditions of induction of microsomal enzymes is associated with a more pronounced bile-expelling effect than their being administered separately. Stimulating effect of oxafenamide on bile production occurs against the background of phenobarbital induction of microsomal enzymes and is not found if the drug is used together with cordiamine. Administration of oxafenamide in the presence of inhibition of bile production induced by cimetidine does not result in normalization of this function of the liver.

Animals↗
PubMedDate not supplied

[The role of bile acids in the regulation of human gallbladder filling].

An artificial increase of a pool of bile acids due to administration of dehydrocholic, chenodesoxycholic acid preparations and dry bile in 22 healthy people and 179 patients with chronic cholecystitis has been studied for its effect on regulation of the gallbladder filling on an empty stomach using daily echocholecystometry. Filling of the gallbladder under artificial sequestration of bile acids during duodenal probing, enterosorption and cholatogenic diarrhea was studied in 55 patients with cholecystitis. It has been proved that an increase of the pool of bile acids induces intensification of the gallbladder filling on an empty stomach, while a decrease of the pool, vice versa, causes attenuation of its filling. It is found out a size of a pool of bile acids in the human organism is an important humoral factor in the physiological mechanism of the gallbladder filling regulation.

Adolescent↗
PubMed1983

Effects of sodium ursodeoxycholate, hyodeoxycholate and dehydrocholate on cholesterol and bile acid metabolism in rats.

Effects of sodium ursodeoxycholate, hyodeoxycholate and dehydrocholate on serum and liver cholesterol levels, bile flow, biliary cholesterol, phospholipid and bile acid secretions, and fecal sterol and bile acid excretions were examined with Wistar strain male rats fed ordinary and 2% cholesterol supplemented diets. Dehydrocholate increased the liver cholesterol level, bile flow and biliary lipid secretion, but ursodeoxycholate and hyodeoxycholate did not. The serum cholesterol level was not changed by the treatments. Ursodeoxycholate and hyodeoxycholate increased their own secretion into the bile and decreased cholic acid secretion, while dehydrocholate increased deoxycholic acid and oxo bile acid secretion. Ursodeoxycholate increased but dehydrocholate decreased the fecal sterol excretion, and hyodeoxycholate caused no change. Dehydrocholate decreased the fecal coprostanol level. The total amounts of the fecal bile acids were similar in all the treated groups, but ursodeoxycholate increased lithocholic acid, alpha, beta- and omega-muricholic acids and ursodeoxycholic acid; hyodeoxycholate increased hyodeoxycholic acid, 3 alpha, 7 beta, 12 alpha-trihydroxy-5 beta-cholanoic acid and oxo bile acids; and dehydrocholate increased deoxycholic acid, cholic acid, omega-muricholic acid and oxo bile acids and decreased hyodeoxycholic acid. These data suggested that ursodeoxycholate was transformed into lithocholic and muricholic acids, and dehydrocholate into cholic and deoxycholic acids during the enterohepatic circulation, but hyodeoxycholate showed almost no change. Ursodeoxycholate and hyodeoxycholate caused neither accumulation of cholesterol in tissues nor increase in bile flow and biliary lipid secretion as well as chenodeoxycholate did. The biological effect of dehydrocholate was similar to that of cholate, and this was partially due to its conversion into cholic acid and deoxycholic acid.

Animals↗
PubMed1993

Importance of high-density lipoprotein-phosphatidylcholine in secretion of phospholipid and cholesterol in bile.

The purpose of this work was to evaluate biliary phosphatidylcholine (PC) secretion after intravenous infusion of high density lipoprotein (HDL)-[3H]phosphatidylcholine (HDL-[3H]PC) in rats and to study the effect of infusion of dehydrocholic and cholic acids, which, respectively, inhibit and stimulate biliary secretion of PC. The data obtained in this study showed that, in the basal state, HDL-PC accounted for 38% of biliary PC. Dehydrocholic acid infusion caused only a "residual" secretion of HDL-PC in the bile; however, cholic acid infusion stimulated the secretion of HDL-PC as well as PC from intrahepatic microsomes. The low level of radioactivity of HDL-PC in intrahepatic compartments suggests that HDL-PC taken up by the liver is predestined for the bile secretion. The correlation between the kinetics of bile secretion of HDL-cholesterol and HDL-[3H]PC suggests the importance of HDL-PC in reverse transport of cholesterol to the liver and its transport to the bile. The differences between the effects of dehydrocholic acid and cholic acid infusions can be explained by the differences in bile salts binding to the surface of HDL.

Animals↗