http://purl.uniprot.org/citations/9323588 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
http://purl.uniprot.org/citations/9323588 | http://www.w3.org/2000/01/rdf-schema#comment | "To determine the physiological role of apolipoprotein (apo) A-IV, knockout mice were created by gene targeting in embryonic stem cells. In apoA-IV knockout mice, plasma cholesterol and triglyceride levels were reduced 25% and 44%, respectively, compared with controls. These changes were accounted for by decreased high density (HDL) and very low density lipoprotein (VLDL) levels, respectively, and metabolic studies indicated increased HDL-cholesteryl ester (CE) fractional catabolic rate (FCR) and reduced VLDL transport rate (TR), respectively. ApoA-IV knockout mice had greater than 70% reductions in both hepatic and intestinal apoC-III RNA levels and a similar reduction in the plasma apoC-III level. Complementation analysis, via crossbreeding of a mouse apoC-III transgene onto both the normal and apoA-IV knockout backgrounds, clearly demonstrated that the low triglyceride (VLDL) level in the apoA-IV knockout mice was due to alterations in apoC-III and not apoA-IV. ApoA-IV knockout mice had normal growth, feeding behavior, and lipid absorption, except male mice showed increased food intake in the 2 h after an 18-h fast, suggesting that under some circumstances apoA-IV might serve as a satiety factor. In summary, studies in apoA-IV-induced mutant mice have demonstrated a role for apoA-IV in increasing HDL cholesterol by inhibiting HDL cholesteryl ester FCR yet argue against the apolipoprotein as an overall important mediator of lipid absorption/metabolism."xsd:string |
http://purl.uniprot.org/citations/9323588 | http://purl.uniprot.org/core/author | "Wu L."xsd:string |
http://purl.uniprot.org/citations/9323588 | http://purl.uniprot.org/core/author | "Breslow J.L."xsd:string |
http://purl.uniprot.org/citations/9323588 | http://purl.uniprot.org/core/author | "Aalto-Setala K."xsd:string |
http://purl.uniprot.org/citations/9323588 | http://purl.uniprot.org/core/author | "Bisgaier C.L."xsd:string |
http://purl.uniprot.org/citations/9323588 | http://purl.uniprot.org/core/author | "Hayek T."xsd:string |
http://purl.uniprot.org/citations/9323588 | http://purl.uniprot.org/core/author | "Sehayek E."xsd:string |
http://purl.uniprot.org/citations/9323588 | http://purl.uniprot.org/core/author | "Merkel M."xsd:string |
http://purl.uniprot.org/citations/9323588 | http://purl.uniprot.org/core/author | "Essenburg A.D."xsd:string |
http://purl.uniprot.org/citations/9323588 | http://purl.uniprot.org/core/author | "Weinstock P.H."xsd:string |
http://purl.uniprot.org/citations/9323588 | http://purl.uniprot.org/core/author | "Sheiffele P."xsd:string |
http://purl.uniprot.org/citations/9323588 | http://purl.uniprot.org/core/date | "1997"xsd:gYear |
http://purl.uniprot.org/citations/9323588 | http://purl.uniprot.org/core/name | "J Lipid Res"xsd:string |
http://purl.uniprot.org/citations/9323588 | http://purl.uniprot.org/core/pages | "1782-1794"xsd:string |
http://purl.uniprot.org/citations/9323588 | http://purl.uniprot.org/core/title | "Decreased HDL cholesterol levels but normal lipid absorption, growth, and feeding behavior in apolipoprotein A-IV knockout mice."xsd:string |
http://purl.uniprot.org/citations/9323588 | http://purl.uniprot.org/core/volume | "38"xsd:string |
http://purl.uniprot.org/citations/9323588 | http://www.w3.org/2004/02/skos/core#exactMatch | http://purl.uniprot.org/pubmed/9323588 |
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