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Article: Oleic acid-induced cholelithiasis in the rabbit: Conversion of dietary oleic acid to cholestanol as a cause of calcium-bile salt gallstones

TitleOleic acid-induced cholelithiasis in the rabbit: Conversion of dietary oleic acid to cholestanol as a cause of calcium-bile salt gallstones
Authors
Issue Date1987
PublisherJohn Wiley & Sons, Inc. The Journal's web site is located at http://www.hepatology.org/
Citation
Hepatology, 1987, v. 7 n. 3, p. 529-534 How to Cite?
AbstractRabbits fed a diet rich in oleic acid develop gallstones consisting of calcium salts of (5α)-glyco-allodeoxycholic acid. To study the metabolic pathway of oleic acid, we followed the changes in plasma, hepatic and biliary lipids in this animal model. In addition, to also determine the role played by intestinal microflora on biliary lipid metabolism, we added kanamycin to the oleic acid diet. Oleic acid-fed rabbits rapidly developed hypercholesterolemia. This was associated with an increase in liver 3-hydroxy-3-methylglutaryl coenzyme A reductase activity, accumulation of cholesterol as well as cholestanol in the liver and progressive saturation of cholesterol in bile. [14C]oleic acid fed orally to rabbits was recovered in liver extracts as both cholesterol and cholestanol. With oleic acid feeding, there was a progressive increase in glyco-allodeoxycholic acid culminating in the formation of gallstones. Kanamycin supplement to the oleic acid diet resulted in the same changes in plasma and hepatic sterol metabolism compared with oleic acid-fed rabbits. There was, however, a striking difference in the biliary bile acid profile. Kanamycin supplementation dramatically reduced the proportion of 5α-dihydroxy bile acids, increased the proportion of 5β-trihydroxy bile acids and completely abolished gallstone formation. We postulate that, in the rabbit, oleic acid is used as a carbon source for cholesterol synthesis, and a high oleic acid diet increases hepatic cholesterogenesis. Hepatic cholesterol is then metabolized to form cholestanol, followed by (5α)-glyco-allocholic acid which is secreted into bile and transformed by gut bacteria to form (5α)-allodeoxycholic acid. Kanamycin abolished gallstone formation by inhibiting intestinal bacterial dehydroxylation.
Persistent Identifierhttp://hdl.handle.net/10722/175647
ISSN
2015 Impact Factor: 11.711
2015 SCImago Journal Rankings: 4.752
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorLee, SPen_US
dc.contributor.authorTasmanJones, Cen_US
dc.contributor.authorCarlisle, VFen_US
dc.date.accessioned2012-11-26T09:00:15Z-
dc.date.available2012-11-26T09:00:15Z-
dc.date.issued1987en_US
dc.identifier.citationHepatology, 1987, v. 7 n. 3, p. 529-534en_US
dc.identifier.issn0270-9139en_US
dc.identifier.urihttp://hdl.handle.net/10722/175647-
dc.description.abstractRabbits fed a diet rich in oleic acid develop gallstones consisting of calcium salts of (5α)-glyco-allodeoxycholic acid. To study the metabolic pathway of oleic acid, we followed the changes in plasma, hepatic and biliary lipids in this animal model. In addition, to also determine the role played by intestinal microflora on biliary lipid metabolism, we added kanamycin to the oleic acid diet. Oleic acid-fed rabbits rapidly developed hypercholesterolemia. This was associated with an increase in liver 3-hydroxy-3-methylglutaryl coenzyme A reductase activity, accumulation of cholesterol as well as cholestanol in the liver and progressive saturation of cholesterol in bile. [14C]oleic acid fed orally to rabbits was recovered in liver extracts as both cholesterol and cholestanol. With oleic acid feeding, there was a progressive increase in glyco-allodeoxycholic acid culminating in the formation of gallstones. Kanamycin supplement to the oleic acid diet resulted in the same changes in plasma and hepatic sterol metabolism compared with oleic acid-fed rabbits. There was, however, a striking difference in the biliary bile acid profile. Kanamycin supplementation dramatically reduced the proportion of 5α-dihydroxy bile acids, increased the proportion of 5β-trihydroxy bile acids and completely abolished gallstone formation. We postulate that, in the rabbit, oleic acid is used as a carbon source for cholesterol synthesis, and a high oleic acid diet increases hepatic cholesterogenesis. Hepatic cholesterol is then metabolized to form cholestanol, followed by (5α)-glyco-allocholic acid which is secreted into bile and transformed by gut bacteria to form (5α)-allodeoxycholic acid. Kanamycin abolished gallstone formation by inhibiting intestinal bacterial dehydroxylation.en_US
dc.languageengen_US
dc.publisherJohn Wiley & Sons, Inc. The Journal's web site is located at http://www.hepatology.org/en_US
dc.relation.ispartofHepatologyen_US
dc.subject.meshAnimalsen_US
dc.subject.meshBile - Metabolismen_US
dc.subject.meshCholelithiasis - Etiology - Metabolismen_US
dc.subject.meshCholestanols - Metabolismen_US
dc.subject.meshCholesterol - Blooden_US
dc.subject.meshFemaleen_US
dc.subject.meshHydroxymethylglutaryl Coa Reductases - Metabolismen_US
dc.subject.meshLiver - Metabolismen_US
dc.subject.meshMaleen_US
dc.subject.meshOleic Acids - Metabolismen_US
dc.subject.meshRabbitsen_US
dc.subject.meshSterols - Metabolismen_US
dc.subject.meshTime Factorsen_US
dc.titleOleic acid-induced cholelithiasis in the rabbit: Conversion of dietary oleic acid to cholestanol as a cause of calcium-bile salt gallstonesen_US
dc.typeArticleen_US
dc.identifier.emailLee, SP: sumlee@hku.hken_US
dc.identifier.authorityLee, SP=rp01351en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1002/hep.1840070319-
dc.identifier.pmid3570164-
dc.identifier.scopuseid_2-s2.0-0023238068en_US
dc.identifier.volume7en_US
dc.identifier.issue3en_US
dc.identifier.spage529en_US
dc.identifier.epage534en_US
dc.identifier.isiWOS:A1987H406200018-
dc.publisher.placeUnited Statesen_US
dc.identifier.scopusauthoridLee, SP=7601417497en_US
dc.identifier.scopusauthoridTasmanJones, C=7003303326en_US
dc.identifier.scopusauthoridCarlisle, VF=6602101145en_US

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