Enrichment of canalicular membrane with cholesterol and sphingomyelin prevents bile salt-induced hepatic damage

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dc.contributor.authorAmigo, L
dc.contributor.authorMendoza, H
dc.contributor.authorZanlungo, S
dc.contributor.authorMiquel, JF
dc.contributor.authorRigotti, A
dc.contributor.authorGonzalez, S
dc.contributor.authorNervi, F
dc.date.accessioned2024-01-10T13:48:05Z
dc.date.available2024-01-10T13:48:05Z
dc.date.issued1999
dc.description.abstractThese studies were undertaken to characterize the role of plasma membrane cholesterol in canalicular secretory functions and hepatocyte integrity against intravenous taurocholate administration. Cholesterol and sphingomyelin concentrations and cholesterol/phospholipid ratios were significantly increased in canalicular membranes of diosgenin-fed rats, suggesting a more resistant structure against solubilization by taurocholate. During taurocholate infusion, control rats had significantly decreased bile flow, whereas diosgenin-fed animals maintained bile flow, Maximal cholesterol output increased by 176% in diosgenin-fed rats, suggesting an increased precursor pool of biliary cholesterol in these animals. Maximal phospholipid output only increased by 43% in diosgenin-fed rats, whereas bile salt output remained at control levels. The kinetics of glutamic oxalacetic: transaminase, lactic dehydrogenase, and alkaline phosphatase activities in bile showed a significantly faster release in control than in diosgenin-fed rats, After 30 min of hp travenous taurocholate infusion, necrotic hepatocytes were significantly increased in control animals.jlr Preservation of bile secretory functions and hepatocellular cytoprotection by diosgenin against the intravenous infusion of toxic doses of taurocholate was associated with an increased concentration of cholesterol and sphingomyelin in the canalicular membrane. The increase of biliary cholesterol output induced by diosgenin was correlated to the enhanced concentration of cholesterol in the canalicular membrane.
dc.format.extent10 páginas
dc.fuente.origenWOS
dc.identifier.eissn1539-7262
dc.identifier.issn0022-2275
dc.identifier.pubmedidMEDLINE:10064742
dc.identifier.urihttps://repositorio.uc.cl/handle/11534/79333
dc.identifier.wosidWOS:000078967800019
dc.information.autorucMedicina;González S;S/I;99856
dc.information.autorucMedicina;Miquel J;S/I;72216
dc.information.autorucMedicina;Nervi F;S/I;99156
dc.information.autorucMedicina;Rigotti A;S/I;68489
dc.issue.numero3
dc.language.isoen
dc.nota.accesoSin adjunto
dc.pagina.final542
dc.pagina.inicio533
dc.publisherAMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC
dc.revistaJOURNAL OF LIPID RESEARCH
dc.rightsregistro bibliográfico
dc.subjectbiliary lipids
dc.subjectcholesterol
dc.subjectbile salts
dc.subjectplasma membrane
dc.subjectmembrane lipids
dc.subjectcanaliculus
dc.subjectcytoprotection
dc.subjectsphingomyelin
dc.subjectmaximal secretory rates
dc.subjectdiosgenin
dc.subjectBILIARY LIPID SECRETION
dc.subjectSTEROL CARRIER PROTEIN-2
dc.subjectP-GLYCOPROTEIN GENE
dc.subjectRAT-LIVER
dc.subjectHOMOZYGOUS DISRUPTION
dc.subjectPLASMA-MEMBRANE
dc.subjectCELL-DAMAGE
dc.subjectTRANSPORT
dc.subjectMETABOLISM
dc.subjectMDR2
dc.subject.ods03 Good Health and Well-being
dc.subject.odspa03 Salud y bienestar
dc.titleEnrichment of canalicular membrane with cholesterol and sphingomyelin prevents bile salt-induced hepatic damage
dc.typeartículo
dc.volumen40
sipa.codpersvinculados99856
sipa.codpersvinculados72216
sipa.codpersvinculados99156
sipa.codpersvinculados68489
sipa.indexWOS
sipa.indexScopus
sipa.trazabilidadCarga SIPA;09-01-2024
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