http://purl.uniprot.org/citations/11590213 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
http://purl.uniprot.org/citations/11590213 | http://www.w3.org/2000/01/rdf-schema#comment | "Previous studies with hypertriglyceridemic APOC3 transgenic mice have suggested that apolipoprotein C-III (apoC-III) may inhibit either the apoE-mediated hepatic uptake of TG-rich lipoproteins and/or the lipoprotein lipase (LPL)-mediated hydrolysis of TG. Accordingly, apoC3 knockout (apoC3(-/-)) mice are hypotriglyceridemic. In the present study, we attempted to elucidate the mechanism(s) underlying these phenomena by intercrossing apoC3(-/-) mice with apoE(-/-) mice to study the effects of apoC-III deficiency against a hyperlipidemic background. Similar to apoE(+/+) apoC3(-/-) mice, apoE(-/-)apoC3(-/-) mice exhibited a marked reduction in VLDL cholesterol and TG, indicating that the mechanism(s) by which apoC-III deficiency exerts its lipid-lowering effect act independent of apoE. On both backgrounds, apoC3(-/-) mice showed normal intestinal lipid absorption and hepatic VLDL TG secretion. However, turnover studies showed that TG-labeled emulsion particles were cleared much more rapidly in apoC3(-/-) mice, whereas the clearance of VLDL apoB, as a marker for whole particle uptake by the liver, was not affected. Furthermore, it was shown that cholesteryl oleate-labeled particles were also cleared faster in apoC3(-/-) mice. Thus the mechanisms underlying the hypolipidemia in apoC3(-/-) mice involve both a more efficient hydrolysis of VLDL TG as well as an enhanced selective clearance of VLDL cholesteryl esters from plasma. In summary, our studies of apoC3(-/-) mice support the concept that apoC-III is an effective inhibitor of VLDL TG hydrolysis and reveal a potential regulating role for apoC-III with respect to the selective uptake of cholesteryl esters."xsd:string |
http://purl.uniprot.org/citations/11590213 | http://purl.uniprot.org/core/author | "van Berkel T.J."xsd:string |
http://purl.uniprot.org/citations/11590213 | http://purl.uniprot.org/core/author | "Dahlmans V.E."xsd:string |
http://purl.uniprot.org/citations/11590213 | http://purl.uniprot.org/core/author | "Havekes L.M."xsd:string |
http://purl.uniprot.org/citations/11590213 | http://purl.uniprot.org/core/author | "Jong M.C."xsd:string |
http://purl.uniprot.org/citations/11590213 | http://purl.uniprot.org/core/author | "Rensen P.C."xsd:string |
http://purl.uniprot.org/citations/11590213 | http://purl.uniprot.org/core/author | "van der Boom H."xsd:string |
http://purl.uniprot.org/citations/11590213 | http://purl.uniprot.org/core/date | "2001"xsd:gYear |
http://purl.uniprot.org/citations/11590213 | http://purl.uniprot.org/core/name | "J Lipid Res"xsd:string |
http://purl.uniprot.org/citations/11590213 | http://purl.uniprot.org/core/pages | "1578-1585"xsd:string |
http://purl.uniprot.org/citations/11590213 | http://purl.uniprot.org/core/title | "Apolipoprotein C-III deficiency accelerates triglyceride hydrolysis by lipoprotein lipase in wild-type and apoE knockout mice."xsd:string |
http://purl.uniprot.org/citations/11590213 | http://purl.uniprot.org/core/volume | "42"xsd:string |
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