scholarly journals Speed of change in biliary lipids and bile acids with chenodeoxycholic acid--is intermittent therapy feasible?

Gut ◽  
1977 ◽  
Vol 18 (1) ◽  
pp. 7-15 ◽  
Author(s):  
J H Iser ◽  
G M Murphy ◽  
R H Dowling
1978 ◽  
Vol 16 (18) ◽  
pp. 69-71

Chenodeoxycholic acid (CDCA) (Chendol - Weddel) is one of two naturally occurring ‘primary’ bile acids (the other being cholic acid) made in the liver from cholesterol. CDCA is synthesised commercially from cholic acid and prescribed as gelatin-coated capsules containing 125 mg CDCA.


1986 ◽  
Vol 79 (9) ◽  
pp. 522-527 ◽  
Author(s):  
Xu Guorong ◽  
C J C Kirk ◽  
A W Goode

Changes in biliary concentrations of bile acids, phospholipids and cholesterol and biliary pressures were measured in dogs. These parameters were studied during 7-day periods of partial biliary obstruction, of varying degrees, and after 24-hour and 48-hour periods of complete obstruction. The samples were obtained via an exteriorized but intact enterohepatic circulation allowing the introduction of varying degrees of obstruction and bile sampling. Biliary obstruction reduced the concentration of all biliary lipids especially when the obstruction produced pressures in excess of 75% of the maximum biliary secretion pressure. Only immediately after the release of a 48-hour period of complete obstruction did the risk of cholesterol supersaturation of bile occur. However, at that time there was a greatly reduced concentration of lipids in the bile and the amount of cholesterol that could potentially have precipitated was very small. It is suggested that this supersaturation would not play a significant role in the formation of gallstones.


1979 ◽  
Vol 25 (2) ◽  
pp. 264-268 ◽  
Author(s):  
O Mäentausta ◽  
O Jänne

Abstract We describe a method for radioimmunoassay of conjugated cholic acid, chenodeoxycholic acid, and deoxycholic acid in serum. In the method, 125I-labeled bile acid conjugates are used as the tracers along with antibodies raised against individual bile acid-bovine serum albumin conjugates. Antibody-bound and free bile acids were separated by polyethylene glycol precipitation (final concentration, 125 g/L). Before radioimmunoassay, 0.1-mL serum samples were precipitated with nine volumes of ethanol, and portions from the supernate were used in the assays. The lowest measurable amounts of the bile acids, expressed as pmol/tube, were: cholic acid conjugates, 2; chenodeoxycholic acid conjugates, 0.5; and deoxycholic acid conjugates. 2. Analytical recovery of bile acids added to bile acid-free serum ranged from 85 to 110%; intra-assay and inter-assay CVs ranged from 3.2 to 5.3% and from 5.3 to 12.2%, respectively. Concentrations (mean +/- SD) of the bile acid conjugates in serum from apparently healthy women and men (in mumol/L) were: cholic acid conjugates, 0.43 +/- 0.17 (n = 126); chenodeoxycholic acid conjugates, 0.47 +/- 0.23 (n = 111); and deoxycholic acid conjugates, 0.33 +/- 0.11 (n = 96). The values for primary bile acids were greatly increased in patients with various hepatobiliary diseases.


1977 ◽  
Vol 73 (2) ◽  
pp. 285-290 ◽  
Author(s):  
S.W. Schalm ◽  
G.P. van Berge-Henegouwen ◽  
A.F. Hofmann ◽  
A.E. Cowen ◽  
J. Turcotte

1976 ◽  
Vol 231 (3) ◽  
pp. 734-742 ◽  
Author(s):  
J Reichen ◽  
G Paumgartner

The uptake of 14C-labeled cholic, taurocholic, and chenodeoxycholic acid by the perfused rat liver was studied to characterize the mechanism responsible for hepatic uptake of bile acids. A rapid-injection multiple indicator-dilution technique and the three-compartment model of Goresky were employed. The kinetics of hepatic uptake of the three bile acids could be described by the Michaelis-Menten equation. The maximal uptake velocities (Vmax) were 24.9 +/- 2.2 (mean +/- SD), 20.8 +/- 1.2, 1.2, and 11.4 +/- 0.9 nmol/s-g liver for cholic, taurocholic, and chenodeoxycholic acid, respectively. The corresponding apparent half-saturation constants (Km) were 526 +/- 125, 258 +/- 43, and 236 +/- 48 nmol/g liver. Competitive inhibition could be demonstrated between cholate and taurocholate as well as between cholate and chenodeoxycholate. Substitution of 94% of the Na+ in the perfusion medium decreased the Vmax and the apparent Km of taurocholate uptake by 68 and 55%, respectively. These findings are consistent with the hypothesis that bile acids are taken up into the hepatocyte by Na+-dependent carrier-mediated transport.


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