Hepatic overexpression of sterol carrier protein-2 inhibits VLDL production and reciprocally enhances biliary lipid secretion

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dc.contributor.authorAmigo, L
dc.contributor.authorZanlungo, S
dc.contributor.authorMiquel, JF
dc.contributor.authorGlick, JM
dc.contributor.authorHyogo, H
dc.contributor.authorCohen, DE
dc.contributor.authorRigotti, A
dc.contributor.authorNervi, F
dc.date.accessioned2024-01-10T12:05:48Z
dc.date.available2024-01-10T12:05:48Z
dc.date.issued2003
dc.description.abstractWe examined in vivo a role for sterol carrier protein-2 (SCP-2) in the regulation of lipid secretion across the hepatic sinusoidal and canalicular membranes. Recombinant adenovirus Ad.rSCP2 was used to overexpress SCP-2 in livers of mice. We determined plasma, hepatic, and biliary lipid concentrations; hepatic fatty acid (FA) and cholesterol synthesis; hepatic and biliary phosphatidylcholine (PC) molecular species; and VLDL triglyceride production. In Ad.rSCP2 mice, there was marked inhibition of hepatic fatty acids and cholesterol synthesis to <62% of control mice. Hepatic triglyceride contents were decreased, while cholesterol and phospholipids concentrations were elevated in Ad.rSCP2 mice. Hepatic VLDL triglyceride production fell in Ad.rSCP2 mice to 39% of control values. As expected, biliary cholesterol, phospholipids, bile acids outputs, and biliary PC hydrophobic index were significantly increased in Ad.rSCP2 mice. These studies indicate that SCP-2 overexpression in the liver markedly inhibits lipid synthesis as well as VLDL production, and alters hepatic lipid contents. In contrast, SCP-2 increased biliary lipid secretion and the proportion of hydrophobic PC molecular species in bile. These effects suggest a key regulatory role for SCP-2 in hepatic lipid metabolism and the existence of a reciprocal relationship between the fluxes of lipids across the sinusoidal and canalicular membranes.
dc.description.funderNIDDK NIH HHS
dc.description.funderNATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES
dc.fechaingreso.objetodigital2024-05-15
dc.format.extent9 páginas
dc.fuente.origenWOS
dc.identifier.doi10.1194/jlr.M200306-JLR200
dc.identifier.eissn1539-7262
dc.identifier.issn0022-2275
dc.identifier.pubmedidMEDLINE:12576522
dc.identifier.urihttps://doi.org/10.1194/jlr.M200306-JLR200
dc.identifier.urihttps://repositorio.uc.cl/handle/11534/76070
dc.identifier.wosidWOS:000181246000018
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.numero2
dc.language.isoen
dc.nota.accesocontenido completo
dc.pagina.final407
dc.pagina.inicio399
dc.publisherAMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC
dc.revistaJOURNAL OF LIPID RESEARCH
dc.rightsacceso abierto
dc.subjecthepatic lipid metabolism
dc.subjectbile
dc.subjectSCP-2
dc.subjectCHOLESTEROL SECRETION
dc.subjectACID SYNTHESIS
dc.subjectGENE-TRANSFER
dc.subjectFATTY-ACIDS
dc.subjectBILE
dc.subjectMEMBRANE
dc.subjectRAT
dc.subjectMETABOLISM
dc.subjectTRIGLYCERIDE
dc.subjectMOUSE
dc.subject.ods03 Good Health and Well-being
dc.subject.odspa03 Salud y bienestar
dc.titleHepatic overexpression of sterol carrier protein-2 inhibits VLDL production and reciprocally enhances biliary lipid secretion
dc.typeartículo
dc.volumen44
sipa.codpersvinculados72216
sipa.codpersvinculados99156
sipa.codpersvinculados68489
sipa.codpersvinculados72650
sipa.indexWOS
sipa.indexScopus
sipa.trazabilidadCarga SIPA;09-01-2024
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