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dc.contributor.authorNeuger, Lucynacat
dc.contributor.authorVilaró, Senén, 1956-2005cat
dc.contributor.authorLópez Iglesias, Carmencat
dc.contributor.authorGupta, Jitendracat
dc.contributor.authorOlivecrona, Thomascat
dc.contributor.authorOlivecrona, Gunillacat
dc.date.accessioned2009-03-20T13:26:37Z-
dc.date.available2009-03-20T13:26:37Z-
dc.date.issued2004cat
dc.identifier.issn1472-6793cat
dc.identifier.urihttp://hdl.handle.net/2445/7281-
dc.description.abstractBACKGROUND: Lipoprotein lipase (LPL) is anchored at the vascular endothelium through interaction with heparan sulfate. It is not known how this enzyme is turned over but it has been suggested that it is slowly released into blood and then taken up and degraded in the liver. Heparin releases the enzyme into the circulating blood. Several lines of evidence indicate that this leads to accelerated flux of LPL to the liver and a temporary depletion of the enzyme in peripheral tissues. RESULTS: Rat livers were found to contain substantial amounts of LPL, most of which was catalytically inactive. After injection of heparin, LPL mass in liver increased for at least an hour. LPL activity also increased, but not in proportion to mass, indicating that the lipase soon lost its activity after being bound/taken up in the liver. To further study the uptake, bovine LPL was labeled with 125I and injected. Already two min after injection about 33 % of the injected lipase was in the liver where it initially located along sinusoids. With time the immunostaining shifted to the hepatocytes, became granular and then faded, indicating internalization and degradation. When heparin was injected before the lipase, the initial immunostaining along sinusoids was weaker, whereas staining over Kupffer cells was enhanced. When the lipase was converted to inactive before injection, the fraction taken up in the liver increased and the lipase located mainly to the Kupffer cells. CONCLUSIONS: This study shows that there are heparin-insensitive binding sites for LPL on both hepatocytes and Kupffer cells. The latter may be the same sites as those that mediate uptake of inactive LPL. The results support the hypothesis that turnover of endothelial LPL occurs in part by transport to and degradation in the liver, and that this transport is accelerated after injection of heparin.eng
dc.format.extent13 p.cat
dc.format.mimetypeapplication/pdf-
dc.language.isoengeng
dc.publisherBioMed Centralcat
dc.relation.isformatofReproducció del document publicat a http://dx.doi.org/10.1186/1472-6793-4-13cat
dc.relation.ispartofBMC Physiology, 2004, vol. 4, núm. 13cat
dc.relation.urihttp://dx.doi.org/10.1186/1472-6793-4-13-
dc.rightscc-by, (c) Neuger et al., 2004cat
dc.rights.urihttp://creativecommons.org/licenses/by/2.0/cat
dc.subject.classificationHeparinacat
dc.subject.classificationLipasescat
dc.subject.classificationFetgecat
dc.subject.classificationRates (Animals de laboratori)cat
dc.subject.otherHeparineng
dc.subject.otherLipoprotein Lipaseeng
dc.subject.otherRatseng
dc.subject.otherLivereng
dc.titleEffects of heparin on the uptake of lipoprotein lipase in rat livereng
dc.typeinfo:eu-repo/semantics/articleeng
dc.typeinfo:eu-repo/semantics/publishedVersion-
dc.identifier.idgrec520353cat
dc.rights.accessRightsinfo:eu-repo/semantics/openAccess-
Appears in Collections:Articles publicats en revistes (Biologia Cel·lular, Fisiologia i Immunologia)

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