Biliary lipid secretion, bile acid metabolism, and gallstone formation are not impaired in hepatic lipase-deficient mice

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dc.contributor.authorAmigo, L
dc.contributor.authorMardones, P
dc.contributor.authorFerrada, C
dc.contributor.authorZanlungo, S
dc.contributor.authorNervi, F
dc.contributor.authorMiquel, JF
dc.contributor.authorRigotti, A
dc.date.accessioned2024-01-10T12:37:48Z
dc.date.available2024-01-10T12:37:48Z
dc.date.issued2003
dc.description.abstractWhereas hepatic lipase (HL) has been implicated in lipoprotein metabolism and atherosclerosis, its role in controlling biliary lipid physiology has not been reported. This work characterizes plasma lipoprotein cholesterol, hepatic cholesterol content, bile acid metabolism, biliary cholesterol secretion, and gallstone formation in HL-deficient mice and C57BL/6 controls fed standard chow, a cholesterol-supplemented diet, or a lithogenic diet. Compared with C57BL/6 controls, HL knockout mice exhibited increased basal plasma high-density lipoprotein (HDL) cholesterol as well as reduced cholesterol levels transported in large lipoproteins in response to cholesterol-enriched diets. Hepatic cholesterol content and biliary cholesterol secretion of chow-fed HL knockout and wild-type mice were not different and increased similarly in both strains after feeding dietary cholesterol or a lithogenic diet. There were no differences in biliary bile acid secretion, bile acid pool size and composition, or fecal bile acid excretion between HL-deficient and control mice. HL knockout mice had a similar prevalence of gallstone formation as compared with control mice when both strains were fed with a lithogenic diet. In conclusion, the deficiency of HL has no major impact on the availability of lipoprotein-derived hepatic cholesterol for biliary secretion; HL expression is not essential for diet-induced gallstone formation in mice.
dc.fechaingreso.objetodigital2024-04-25
dc.format.extent9 páginas
dc.fuente.origenWOS
dc.identifier.doi10.1053/jhep.2003.50379
dc.identifier.issn0270-9139
dc.identifier.pubmedidMEDLINE:12939599
dc.identifier.urihttps://doi.org/10.1053/jhep.2003.50379
dc.identifier.urihttps://repositorio.uc.cl/handle/11534/76928
dc.identifier.wosidWOS:000185085000022
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.information.autorucMedicina;Zanlungo S;S/I;72650
dc.issue.numero3
dc.language.isoen
dc.nota.accesocontenido parcial
dc.pagina.final734
dc.pagina.inicio726
dc.publisherW B SAUNDERS CO
dc.revistaHEPATOLOGY
dc.rightsacceso restringido
dc.subjectHIGH-DENSITY-LIPOPROTEIN
dc.subjectPERFUSED-RAT-LIVER
dc.subjectRECEPTOR SR-BI
dc.subjectIN-VIVO
dc.subjectCHOLESTEROL SECRETION
dc.subjectAPOLIPOPROTEIN-E
dc.subjectSELECTIVE UPTAKE
dc.subjectTRANSGENIC MICE
dc.subjectHDL
dc.subjectCELLS
dc.subject.ods03 Good Health and Well-being
dc.subject.odspa03 Salud y bienestar
dc.titleBiliary lipid secretion, bile acid metabolism, and gallstone formation are not impaired in hepatic lipase-deficient mice
dc.typeartículo
dc.volumen38
sipa.codpersvinculados72216
sipa.codpersvinculados99156
sipa.codpersvinculados68489
sipa.codpersvinculados72650
sipa.indexWOS
sipa.indexScopus
sipa.trazabilidadCarga SIPA;09-01-2024
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