Hypercholeretic bile acids: A clue to the mechanism?

Erlinger, S

doi:10.1002/hep.1840110527

Cited by 21 publications

(5 citation statements)

References 12 publications

(4 reference statements)

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“…Second, when the synthetically prepared 3-glucuronide was infused into the biliary fistula rat, it did not induce a true hypercholeresis, if hypercholeresis is defined as a bile flow much too great to be explained by the osmotic effect of recovered bile acids and associated with an enrichment in bicarbonate concentration above that of plasma. The synthetic glucuronide, which is a di-anionic compound, had a choleretic activity of 25 p.Vumo1, quite similar to that of several other dianionic compounds (2 1 kl/compound; 7 kl/ion) (33)(34)(35)(36)(37)(38). Furthermore, the bicarbonate concentration of bile did not increase.…”

Section: Discussionmentioning

confidence: 73%

Hypercholeresis induced by unconjugated bile acid infusion correlates with recovery in bile of unconjugated bile acids

et al. 1991

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Using the isolated perfused rat and hamster liver, the relationship between bile flow, bile acid secretion rate and bile acid biotransformation after the injection of a small, bolus dose of radioactive ursodeoxycholate or of its C23 homolog, norursodeoxycholate, was examined. Ursodeoxycholate was promptly secreted into bile mostly as amino acid conjugates; less than 3% was secreted in unchanged form in the rat and less than 2% in the hamster. In contrast, norursodeoxycholate was secreted slowly, and biotransformed into glucuronide conjugates and unconjugated trihydroxy derivatives; it was also secreted in part in unchanged form. In the rat, 7% was secreted in unconjugated trihydroxy derivatives and 3% in unchanged form; in the hamster, 7% was secreted as unconjugated trihydroxy derivatives and 4% in unchanged form. The secreted bile acid species that showed the highest correlation with bile flow by far was always the unconjugated form in both rat and hamster. By multiple regression analysis, the apparent choleretic activity (microliters of induced bile flow per micromoles recovered bile acid molecules) indicated marked hypercholeresis for the unconjugated bile acid marked hypercholeresis for the unconjugated bile acid with values ranging from 100 to 300 microliters/mumol. Bile flow also correlated with total bile acid recovery for ursodeoxycholate in rat and norursodeoxycholate in hamster, but in all studies the apparent choleretic activity was far lower. Other calculations indicated that most bile flow during the first 30 min was induced by secretion of the unconjugated bile acid species in all experiments, the proportion ranging from 50% to 90%. The results indicate that when a bolus of ursodeoxycholate or norursodeoxycholate is presented to the perfused rodent liver, the secretion of the unchanged bile acid appears to be responsible for most of the bile flow, probably by a cholehepatic shunting mechanism.

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Section: Discussionmentioning

confidence: 73%

Hypercholeresis induced by unconjugated bile acid infusion correlates with recovery in bile of unconjugated bile acids

et al. 1991

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“…Indeed, in case 1 biliary obstruction proved to be transient, as attempts to increase bile flow were apparently successful. [13][14][15][16] In cases 3, 5 and 7, gallbladder sludge and stones were more problematic. Case 3 developed pancreatitis and biliary obstruction from gallstones on day 32 post transplant, a time when most patients are resuming oral intake.…”

Section: Discussionmentioning

confidence: 99%

Biliary obstruction in hematopoietic cell transplant recipients: an uncommon diagnosis with specific causes

Murakami

Louie

Chan

et al. 1999

Bone Marrow Transplant

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Summary:Jaundice is a common problem in marrow transplant recipients. The incidence of bile duct obstruction in this setting is unknown. The purpose of this study was to determine the incidence of biliary obstruction, the causes, and outcomes following marrow transplant. Consecutive cases were reviewed at two major transplant centers in the United States from 1969 to 1996 at the Fred Hutchinson Cancer Research Center and 1989 to 1996 at the City of Hope National Medical Center. Nine cases of biliary obstruction were identified as a cause of jaundice in 7412 marrow transplant recipients, an incidence of 0.12%. The presentation was bimodal, with seven cases occurring prior to day 100 and two occurring 2 to 4 years after transplantation. The age distribution was 15 to 50 years and all patients had received allogeneic transplants. The causes of obstruction included gallbladder sludge (n‫,)1؍‬ a duodenal hematoma (n‫,)1؍‬ choledocholithiasis with biliary pancreatitis (n‫,)1؍‬ bile duct infection (n‫,)2؍‬ recurrent malignancy (n‫,)1؍‬ choledocholithiasis associated with a benign stricture (n‫,)1؍‬ Epstein-Barr virus-related lymphoproliferative disorder (n‫,)1؍‬ and a benign stricture of unknown etiology (n‫.)1؍‬ Biliary obstruction is a rare cause of jaundice in the post-transplant period. The presentation was similar to that of other post-transplant hepatobiliary problems, but with disparate causes.

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“…UDCA protects the lipid layer of the liver cell membrane against the toxic effect of hydrophobic bile salts (cytoprotective effect) [13]. It prevents the inclusion of bile acids such as kenodeoxycholic acid and cholic acid in the enterohepatic circulation and constitutes 40% to 55% of total bile salts, resulting in the formation of copious amounts bile rich in bicarbonate (cholehepatic shunt) [14]. Oral administration of various bile salts to obstructive jaundice rats eliminates endotoxemia by reducing intestinal absorption of endotoxin.…”

Section: Discussionmentioning

confidence: 99%

The protective effects of ursodeoxycholic acid and the selective cyclooxygenase-2 inhibitor celecoxib on liver damage in an experimental cholestasis model

Küçük

Öztürk

2019

j-ebr

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Cholestasis leads to liver cell death, fibrosis, cirrhosis, and eventually liver failure. Ursodeoxycholic acid (UDCA) is the only Food and Drug Administration-approved treatment for cholestatic disorders. Hepatic cyclooxygenase-2 (COX-2) expression increases in various chronic liver diseases caused either by viruses or toxins. The present study was conducted to investigate the effects of UDCA and the selective COX-2 inhibitor celecoxib on inflammation and fibrogenesis in a rat model of cholestasis induced by bile duct ligation (BDL). Methods: Fifty Sprague-Dawley rats that underwent common BDL for 21 days were assigned to one of five treatment groups (sham-operation, BDL, daily UDCA treatment following BDL, daily celecoxib treatment following BDL, and daily celecoxib and UDCA combination treatment following BDL). Serum and liver samples were collected after 21 days. Fibrosis, ductular proliferation, and portal inflammation were scored in liver samples. Liver function tests were evaluated. Results: In comparison with the control group, the BDL group showed hepatic damage as evidenced by elevation in serum biochemical and histological changes such as ductular reaction, fibrosis, and inflammation. These pathophysiological changes were attenuated by chronic UDCA and selective COX-2 inhibitor celecoxib supplementation. Conlusion: Our findings indicate that the addition of Celecoxib to UDCA reduces liver inflammation and fibrosis and might be an effective supplemental therapy with UDCA for cholestatic diseases. The beneficial effects of chronic UDCA and Celecoxib supplementation may be associated with their potential cytoprotective, anti-oxidative and anti-inflammatory effects.

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Hypercholeretic bile acids: A clue to the mechanism?

Cited by 21 publications

References 12 publications

Hypercholeresis induced by unconjugated bile acid infusion correlates with recovery in bile of unconjugated bile acids

Hypercholeresis induced by unconjugated bile acid infusion correlates with recovery in bile of unconjugated bile acids

Biliary obstruction in hematopoietic cell transplant recipients: an uncommon diagnosis with specific causes

The protective effects of ursodeoxycholic acid and the selective cyclooxygenase-2 inhibitor celecoxib on liver damage in an experimental cholestasis model

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