Hepatic cholesterol and bile acid metabolism and intestinal cholesterol absorption in scavenger receptor class B type I-deficient mice

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dc.contributor.authorMardones, P
dc.contributor.authorQuinones, V
dc.contributor.authorAmigo, L
dc.contributor.authorMoreno, M
dc.contributor.authorMiquel, JF
dc.contributor.authorSchwarz, M
dc.contributor.authorMiettinen, HE
dc.contributor.authorTrigatti, B
dc.contributor.authorKrieger, M
dc.contributor.authorVanPatten, S
dc.contributor.authorCohen, DE
dc.contributor.authorRigotti, A
dc.date.accessioned2024-01-10T13:49:00Z
dc.date.available2024-01-10T13:49:00Z
dc.date.issued2001
dc.description.abstractThe scavenger receptor class B type I (SR-BI), which is expressed in the liver and intestine, plays a critical role in cholesterol metabolism in rodents. While hepatic SR-BI expression controls high density lipoprotein (HDL) cholesterol metabolism, intestinal SR-BI has been proposed to facilitate cholesterol absorption. To evaluate further the relevance of SR-BI in the enterohepatic circulation of cholesterol and bile salts, we studied biliary lipid secretion, hepatic sterol content and synthesis, bile acid metabolism, fecal neutral sterol excretion, and intestinal cholesterol absorption in SR-BI knockout mice. SR-BI deficiency selectively impaired biliary cholesterol secretion, without concomitant changes in either biliary bile acid or phospholipid secretion. Hepatic total and unesterified cholesterol contents were slightly increased in SR-BI-deficient mice, while sterol synthesis was not significantly changed, Bile acid pool size and composition, as well as fecal bile acid excretion, were not altered in SR-BI knockout mice. Intestinal cholesterol absorption was somewhat increased and fecal sterol excretion was slightly decreased in SR-BI knockout mice relative to controls. These findings establish the critical role of hepatic SR-BI expression in selectively controlling the utilization of HDL cholesterol for biliary secretion. In contrast, SR-BI expression is not essential for intestinal cholesterol absorption.
dc.description.funderNATIONAL HEART, LUNG, AND BLOOD INSTITUTE
dc.description.funderNATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES
dc.description.funderNHLBI NIH HHS
dc.description.funderNIDDK NIH HHS
dc.fechaingreso.objetodigital2024-06-25
dc.format.extent11 páginas
dc.fuente.origenWOS
dc.identifier.issn0022-2275
dc.identifier.pubmedidMEDLINE:11181745
dc.identifier.urihttps://doi.org/10.1016/S0022-2275(20)31676-X
dc.identifier.wosidWOS:000167261100002
dc.information.autorucMedicina;Miquel J;S/I;72216
dc.information.autorucMedicina;Rigotti A;S/I;68489
dc.issue.numero2
dc.language.isoen
dc.nota.accesoContenido completo
dc.pagina.final180
dc.pagina.inicio170
dc.publisherLIPID RESEARCH INC
dc.revistaJOURNAL OF LIPID RESEARCH
dc.rightsacceso abierto
dc.subjectHDL
dc.subjectbiliary lipids
dc.subjectsterol synthesis
dc.subjecthepatic gene expression
dc.subjectcholesterol feeding
dc.subjectHIGH-DENSITY-LIPOPROTEIN
dc.subjectSTEROL CARRIER PROTEIN-2
dc.subjectPERFUSED-RAT-LIVER
dc.subjectALTERS PLASMA HDL
dc.subjectAPOPROTEIN-A-I
dc.subjectSR-BI
dc.subjectSELECTIVE UPTAKE
dc.subjectBILIARY CHOLESTEROL
dc.subjectDIETARY-CHOLESTEROL
dc.subjectTARGETED MUTATION
dc.subject.ods03 Good Health and Well-being
dc.subject.odspa03 Salud y bienestar
dc.titleHepatic cholesterol and bile acid metabolism and intestinal cholesterol absorption in scavenger receptor class B type I-deficient mice
dc.typeartículo
dc.volumen42
sipa.codpersvinculados72216
sipa.codpersvinculados68489
sipa.indexWOS
sipa.indexScopus
sipa.trazabilidadCarga SIPA;09-01-2024
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