Statements in which the resource exists.
SubjectPredicateObjectContext
pubmed-article:16002078rdf:typepubmed:Citationlld:pubmed
pubmed-article:16002078lifeskim:mentionsumls-concept:C0599779lld:lifeskim
pubmed-article:16002078lifeskim:mentionsumls-concept:C0023820lld:lifeskim
pubmed-article:16002078lifeskim:mentionsumls-concept:C0205054lld:lifeskim
pubmed-article:16002078lifeskim:mentionsumls-concept:C0242339lld:lifeskim
pubmed-article:16002078lifeskim:mentionsumls-concept:C0003591lld:lifeskim
pubmed-article:16002078lifeskim:mentionsumls-concept:C0311400lld:lifeskim
pubmed-article:16002078lifeskim:mentionsumls-concept:C0021655lld:lifeskim
pubmed-article:16002078lifeskim:mentionsumls-concept:C1280500lld:lifeskim
pubmed-article:16002078lifeskim:mentionsumls-concept:C0965129lld:lifeskim
pubmed-article:16002078lifeskim:mentionsumls-concept:C0033268lld:lifeskim
pubmed-article:16002078pubmed:issue1lld:pubmed
pubmed-article:16002078pubmed:dateCreated2006-1-25lld:pubmed
pubmed-article:16002078pubmed:abstractTextA novel animal model of insulin resistance, the fructose-fed Syrian golden hamster, was employed to investigate the efficacy and mechanisms of action of rosuvastatin, a HMG-CoA reductase inhibitor, in ameliorating metabolic dyslipidemia in insulin-resistant states. Fructose feeding for a 2-week period induced insulin resistance and a significant increase in hepatic secretion of VLDL. This was followed by a fructose-enriched diet with or without 10 mg/kg rosuvastatin for 14 days. Fructose feeding in the first 2 weeks caused a significant increase in plasma total cholesterol and triglyceride in both groups (n=6, p<0.001). However, there was a significant decline (30%, n=8, p<0.05) in plasma triglyceride levels following rosuvastatin feeding (10 mg/kg). A significant decrease (n=6, p<0.05) was also observed in VLDL-apoB production in hepatocytes isolated from drug-treated hamsters, together with an increased apoB degradation (n=6, p<0.05). Similar results were obtained in parallel cell culture experiments in which primary hepatocytes were first isolated from chow-fed hamsters, and then treated in vitro with 15 microM rosuvastatin for 18 h. Rosuvastatin at 5 microM caused a substantial reduction in synthesis of unesterified cholesterol and cholesterol ester (98 and 25%, n=9, p<0.01 or p<0.05) and secretion of newly synthesized unesterified cholesterol, cholesterol ester, and triglyceride (95, 42, and 60% reduction, respectively, n=9, p<0.01 or p<0.05). This concentration of rosuvastatin also caused a significant reduction (75% decrease, n=4, p<0.01) in the extracellular secretion of VLDL-apoB100, accompanied by a significant increase in the intracellular degradation of apoB100. There was a 12% reduction (not significant, p>0.05) in hepatic MTP and no changes in ER-60 (a chaperone involved in apoB degradation) protein levels. Taken together, these data suggest that the assembly and secretion of VLDL particles in hamster hepatocytes can be acutely inhibited by rosuvastatin in a process involving enhanced apoB degradation. This appears to lead to a significant amelioration of hepatic VLDL-apoB overproduction observed in the fructose-fed, insulin-resistant hamster model.lld:pubmed
pubmed-article:16002078pubmed:languageenglld:pubmed
pubmed-article:16002078pubmed:journalhttp://linkedlifedata.com/r...lld:pubmed
pubmed-article:16002078pubmed:citationSubsetIMlld:pubmed
pubmed-article:16002078pubmed:chemicalhttp://linkedlifedata.com/r...lld:pubmed
pubmed-article:16002078pubmed:chemicalhttp://linkedlifedata.com/r...lld:pubmed
pubmed-article:16002078pubmed:chemicalhttp://linkedlifedata.com/r...lld:pubmed
pubmed-article:16002078pubmed:chemicalhttp://linkedlifedata.com/r...lld:pubmed
pubmed-article:16002078pubmed:chemicalhttp://linkedlifedata.com/r...lld:pubmed
pubmed-article:16002078pubmed:chemicalhttp://linkedlifedata.com/r...lld:pubmed
pubmed-article:16002078pubmed:statusMEDLINElld:pubmed
pubmed-article:16002078pubmed:monthMarlld:pubmed
pubmed-article:16002078pubmed:issn0021-9150lld:pubmed
pubmed-article:16002078pubmed:authorpubmed-author:AdeliKhosrowKlld:pubmed
pubmed-article:16002078pubmed:authorpubmed-author:NaplesMarkMlld:pubmed
pubmed-article:16002078pubmed:authorpubmed-author:CheungRaphael...lld:pubmed
pubmed-article:16002078pubmed:authorpubmed-author:ChongTaryneTlld:pubmed
pubmed-article:16002078pubmed:authorpubmed-author:SmithGraham...lld:pubmed
pubmed-article:16002078pubmed:authorpubmed-author:FedericoLisaLlld:pubmed
pubmed-article:16002078pubmed:authorpubmed-author:TaylorDeniseDlld:pubmed
pubmed-article:16002078pubmed:issnTypePrintlld:pubmed
pubmed-article:16002078pubmed:volume185lld:pubmed
pubmed-article:16002078pubmed:ownerNLMlld:pubmed
pubmed-article:16002078pubmed:authorsCompleteYlld:pubmed
pubmed-article:16002078pubmed:pagination21-31lld:pubmed
pubmed-article:16002078pubmed:dateRevised2006-11-15lld:pubmed
pubmed-article:16002078pubmed:meshHeadingpubmed-meshheading:16002078...lld:pubmed
pubmed-article:16002078pubmed:meshHeadingpubmed-meshheading:16002078...lld:pubmed
pubmed-article:16002078pubmed:meshHeadingpubmed-meshheading:16002078...lld:pubmed
pubmed-article:16002078pubmed:meshHeadingpubmed-meshheading:16002078...lld:pubmed
pubmed-article:16002078pubmed:meshHeadingpubmed-meshheading:16002078...lld:pubmed
pubmed-article:16002078pubmed:meshHeadingpubmed-meshheading:16002078...lld:pubmed
pubmed-article:16002078pubmed:meshHeadingpubmed-meshheading:16002078...lld:pubmed
pubmed-article:16002078pubmed:meshHeadingpubmed-meshheading:16002078...lld:pubmed
pubmed-article:16002078pubmed:meshHeadingpubmed-meshheading:16002078...lld:pubmed
pubmed-article:16002078pubmed:meshHeadingpubmed-meshheading:16002078...lld:pubmed
pubmed-article:16002078pubmed:meshHeadingpubmed-meshheading:16002078...lld:pubmed
pubmed-article:16002078pubmed:meshHeadingpubmed-meshheading:16002078...lld:pubmed
pubmed-article:16002078pubmed:meshHeadingpubmed-meshheading:16002078...lld:pubmed
pubmed-article:16002078pubmed:meshHeadingpubmed-meshheading:16002078...lld:pubmed
pubmed-article:16002078pubmed:meshHeadingpubmed-meshheading:16002078...lld:pubmed
pubmed-article:16002078pubmed:meshHeadingpubmed-meshheading:16002078...lld:pubmed
pubmed-article:16002078pubmed:meshHeadingpubmed-meshheading:16002078...lld:pubmed
pubmed-article:16002078pubmed:meshHeadingpubmed-meshheading:16002078...lld:pubmed
pubmed-article:16002078pubmed:meshHeadingpubmed-meshheading:16002078...lld:pubmed
pubmed-article:16002078pubmed:year2006lld:pubmed
pubmed-article:16002078pubmed:articleTitleEffect of rosuvastatin on hepatic production of apolipoprotein B-containing lipoproteins in an animal model of insulin resistance and metabolic dyslipidemia.lld:pubmed
pubmed-article:16002078pubmed:affiliationDivision of Clinical Biochemistry, Research Institute, Hospital for Sick Children & Department of Laboratory Medicine and Pathobiology, University of Toronto, Toronto, Ont., Canada M5G 1X8.lld:pubmed
pubmed-article:16002078pubmed:publicationTypeJournal Articlelld:pubmed
pubmed-article:16002078pubmed:publicationTypeComparative Studylld:pubmed
pubmed-article:16002078pubmed:publicationTypeResearch Support, Non-U.S. Gov'tlld:pubmed
http://linkedlifedata.com/r...pubmed:referesTopubmed-article:16002078lld:pubmed
http://linkedlifedata.com/r...pubmed:referesTopubmed-article:16002078lld:pubmed
http://linkedlifedata.com/r...pubmed:referesTopubmed-article:16002078lld:pubmed
http://linkedlifedata.com/r...pubmed:referesTopubmed-article:16002078lld:pubmed