Biliary cholesterol saturation and gallstone formation

1998 ◽  
Vol 10 (12) ◽  
pp. A1 ◽  
Author(s):  
K. J. van Erpecum
Keyword(s):  
Gallstone Formation ◽  
Biliary Cholesterol ◽  
Cholesterol Saturation

Enrichment of bile with tauroursodeoxycholic acid and biliary cholesterol saturation in hamsters

1982 ◽  
Vol 243 (5) ◽  
pp. G424-G427
Author(s):  
B. Handelsman ◽  
G. Bonorris ◽  
J. W. Marks ◽  
L. J. Schoenfield
Keyword(s):  
Ursodeoxycholic Acid ◽  
Saturation Index ◽  
Saturation Indices ◽  
Biliary Cholesterol ◽  
Molar Percentage ◽  
Lithogenic Diet ◽  
Cholesterol Saturation ◽  
Before And After ◽  
Ketamine Anesthesia ◽  
Lower Saturation

Three groups of golden Syrian hamsters were fed equimolar amounts of taurine-conjugated ursodeoxycholic acid (TUDCA) or unconjugated ursodeoxycholic acid (UDCA) with or without excess taurine for 2 wk. They also received a lithogenic diet composed of standard rodent chow containing ethynylestradiol and increased cholesterol. Bile was obtained from the gallbladder after ketamine anesthesia and analyzed for biliary lipids. The percentage of biliary UDCA was higher with TUDCA (38.5 +/- 3.7) than with UDCA plus taurine (26.5 +/- 2.0, P less than 0.01). The glycine-to-taurine ratio of biliary UDCA conjugates was lower with TUDCA (0.9 +/- 0.1) than with UDCA plus taurine (2.1 +/- 0.2, P less than 0.01) and was highest with UDCA without taurine (4.1 +/- 0.1, P less than 0.01). Biliary cholesterol (molar percentage) and the cholesterol saturation indices with or without correction for UDCA-rich bile were significantly lower with TUDCA than with unconjugated UDCA with or without added taurine. In conclusion, administration for 2 wk of TUDCA, compared with an equimolar amount of unconjugated UDCA plus taurine, produced in the bile of hamsters a higher percentage of UDCA, a lower glycine-to-taurine ratio of UDCA conjugates, and a lower saturation index before and after adjustment for UDCA-rich bile.

scholarly journals Dietary N-3 polyunsaturated fatty acids decrease biliary cholesterol saturation in gallstone disease

Hepatology ◽  
1992 ◽  
Vol 16 (4) ◽  
pp. 960-967 ◽  
Author(s):  
Frieder Berr ◽  
Joseph Holl ◽  
Dieter Jüngst ◽  
Sven Fischer ◽  
Werner O. Richter ◽  
...  
Keyword(s):  
Fatty Acids ◽  
Polyunsaturated Fatty Acids ◽  
Gallstone Disease ◽  
Biliary Cholesterol ◽  
Cholesterol Saturation

scholarly journals Prolonged large bowel transit increases serum deoxycholic acid: a risk factor for octreotide induced gallstones

Gut ◽  
1999 ◽  
Vol 44 (5) ◽  
pp. 675-681 ◽  
Author(s):  
M J Veysey ◽  
L A Thomas ◽  
A I Mallet ◽  
P J Jenkins ◽  
G M Besser ◽  
...  
Keyword(s):  
Risk Factor ◽  
Large Bowel ◽  
Deoxycholic Acid ◽  
Gallstone Formation ◽  
Intestinal Transit ◽  
Fasting Serum ◽  
Cholesterol Saturation ◽  
Transit Times ◽  
Octreotide Treatment

BACKGROUNDTreatment of acromegaly with octreotide increases the proportion of deoxycholic acid in, and the cholesterol saturation of, bile and induces the formation of gallstones. Prolongation of intestinal transit has been proposed as the mechanism for the increase in the proportion of deoxycholic acid in bile.AIMSTo study the effects of octreotide on intestinal transit in acromegalic patients during octreotide treatment, and to examine the relation between intestinal transit and bile acid composition in fasting serum.METHODSMouth to caecum and large bowel transit times, and the proportion of deoxycholic acid in fasting serum were measured in non-acromegalic controls, acromegalic patients untreated with octreotide, acromegalics on long term octreotide, and patients with simple constipation. Intestinal transit and the proportion of deoxycholic acid were compared in acromegalic patients before and during octreotide.RESULTSAcromegalics untreated with octreotide had longer mouth to caecum and large bowel transit times than controls. Intestinal transit was further prolonged by chronic octreotide treatment. There were significant linear relations between large bowel transit time and the proportion of deoxycholic acid in the total, conjugated, and unconjugated fractions of fasting serum.CONCLUSIONSThese data support the hypothesis that, by prolonging large bowel transit, octreotide increases the proportion of deoxycholic acid in fasting serum (and, by implication, in bile) and thereby the risk of gallstone formation.

scholarly journals Sterol carrier protein 2 participates in hypersecretion of biliary cholesterol during gallstone formation in genetically gallstone-susceptible mice

1998 ◽  
Vol 336 (1) ◽  
pp. 33-37 ◽  
Author(s):  
Michael FUCHS ◽  
Frank LAMMERT ◽  
David Q.-H. WANG ◽  
Beverly PAIGEN ◽  
Martin C. CAREY ◽  
...  
Keyword(s):  
Steady State ◽  
Cholesterol Gallstone ◽  
Gallstone Formation ◽  
Carrier Protein ◽  
Mrna Levels ◽  
Sterol Carrier Protein ◽  
Biliary Cholesterol ◽  
Lithogenic Diet ◽  
Sterol Carrier Protein 2 ◽  
Akr Mice

In inbred mice, susceptibility to cholesterol gallstone disease is conferred by Lith genes, which in part promote hypersecretion of cholesterol into bile in response to a high-fat/cholesterol/cholic acid (lithogenic) diet. Because cytosolic sterol carrier protein 2 (SCP2) is believed to participate in cellular cholesterol trafficking and is elevated in the liver cytosol of cholesterol gallstone patients, we defined the hepatic expression of SCP2 during cholesterol gallstone formation in gallstone-susceptible C57L and gallstone-resistant AKR mice fed the lithogenic diet. Steady-state cytosolic SCP2 levels in C57L, but not AKR mice increased as a function of time and were correlated positively with biliary cholesterol hypersecretion, cholesterol saturation indices of gall-bladder biles and the appearance of liquid and solid cholesterol crystals leading to gallstone formation. Steady-state mRNA levels increased co-ordinately, consistent with regulation of SCP2 expression at the transcriptional level. Our results suggest that overexpression of SCP2 contributes to biliary cholesterol hypersecretion and the pathogenesis of gallstones in genetically susceptible mice. Because of the different chromosomal localizations of the Lith and Scp2 genes, we postulate that Lith genes control SCP2 expression indirectly.

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