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dc.contributor.authorLichtman, Andrew Harry
dc.contributor.authorClinton, S. K.
dc.contributor.authorIiyama, K.
dc.contributor.authorConnelly, P. W.
dc.contributor.authorLibby, Peter
dc.contributor.authorCybulsky, M. I.
dc.date.accessioned2018-03-27T18:34:57Z
dc.date.issued1999
dc.identifier.citationLichtman, A. H., S. K. Clinton, K. Iiyama, P. W. Connelly, P. Libby, and M. I. Cybulsky. 1999. “Hyperlipidemia and Atherosclerotic Lesion Development in LDL Receptor Deficient Mice Fed Defined Semipurified Diets With and Without Cholate.” Arteriosclerosis, Thrombosis, and Vascular Biology 19 (8) (August 1): 1938–1944. doi:10.1161/01.atv.19.8.1938.en_US
dc.identifier.issn1079-5642en_US
dc.identifier.urihttp://nrs.harvard.edu/urn-3:HUL.InstRepos:35140985
dc.description.abstractPast studies of atherosclerosis in mice have used chow-based diets supplemented with cholesterol, lipid, and sodium cholate to overcome species resistance to lesion formation. Similar diets have been routinely used in studies with LDL receptor–deficient (LDLR−/−) mice. The nonphysiological nature and potential toxicity of cholate-containing diets have led to speculation that atherogenesis in these mice may not accurately reflect the human disease process. We have designed a semipurified AIN-76A–based diet that can be fed in powdered, pelleted, or liquid form and manipulated for the precise evaluation of diet–genetic interactions in murine atherosclerosis. LDLR−/− mice were randomly assigned among 4 diets (n=6/diet) as follows: 1, control, 10% kcal lipid; 2, high fat (40% kcal), moderate cholesterol (0.5% by weight); 3, high fat, high cholesterol (1.25% by weight); and 4, high fat, high cholesterol, and 0.5% (wt/wt) sodium cholate. Fasting serum cholesterol was increased in all cholesterol-supplemented mice compared with controls after 6 or 12 weeks of feeding (P<0.01). The total area of oil red O–stained atherosclerotic lesions was determined from digitally scanned photographs. In contrast to the control group, all mice in cholesterol-supplemented dietary groups 2 to 4 had lesions involving 7.01% to 12.79% area of the thoracic and abdominal aorta at 12 weeks (P<0.002, for each group versus control). The distribution pattern of atherosclerotic lesions was highly reproducible and comparable. The histological features of lesions in mice fed cholate-free or cholate-containing diets were similar. This study shows that sodium cholate is not necessary for the formation of atherosclerosis in LDLR−/− mice and that precisely defined semipurified diets are a valuable tool for the examination of diet–gene interactions.en_US
dc.language.isoen_USen_US
dc.publisherOvid Technologies (Wolters Kluwer Health)en_US
dc.relation.isversionofdoi:10.1161/01.ATV.19.8.1938en_US
dc.relation.hasversionhttp://www.ncbi.nlm.nih.gov/pubmed/10446074en_US
dash.licenseMETA_ONLY
dc.subjectatherosclerosisen_US
dc.subjectLDL receptoren_US
dc.subjectdietary lipidsen_US
dc.subjectcholesterolen_US
dc.subjectmiceen_US
dc.titleHyperlipidemia and Atherosclerotic Lesion Development in LDL Receptor Deficient Mice Fed Defined Semipurified Diets With and Without Cholateen_US
dc.typeJournal Articleen_US
dc.description.versionVersion of Recorden_US
dc.relation.journalArteriosclerosis, Thrombosis, and Vascular Biologyen_US
dash.depositing.authorLibby, Peter
dash.embargo.until10000-01-01
dc.identifier.doi10.1161/01.ATV.19.8.1938*
workflow.legacycommentsnoap.needmanen_US
dash.contributor.affiliatedLichtman, Andrew
dash.contributor.affiliatedLibby, Peter
dc.identifier.orcid0000-0002-1502-502X


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