Apolipoprotein E Deficiency Increases Remnant Lipoproteins and Accelerates Progressive Atherosclerosis, But Not Xanthoma Formation, in Gene-Modified Minipigs

Publikation: Bidrag til tidsskriftTidsskriftartikelForskningfagfællebedømt

Jeong Shim, Christian Bo Poulsen, Mette K. Hagensen, Torben Larsen, Peter M.H. Heegaard, Christina Christoffersen, Lars Bolund, Mette Schmidt, Ying Liu, Juan Li, Rong Li, Henrik Callesen, Jacob F. Bentzon, Charlotte B. Sørensen

Deficiency of apolipoprotein E (APOE) causes familial dysbetalipoproteinemia in humans resulting in a higher risk of atherosclerotic disease. In mice, APOE deficiency results in a severe atherosclerosis phenotype, but it is unknown to what extent this is unique to mice. In this study, APOE was targeted in Yucatan minipigs. APOE−/− minipigs displayed increased plasma cholesterol and accumulation of apolipoprotein B-48–containing chylomicron remnants on low-fat diet, which was significantly accentuated upon feeding a high-fat, high-cholesterol diet. APOE−/− minipigs displayed accelerated progressive atherosclerosis but not xanthoma formation. This indicates that remnant lipoproteinemia does not induce early lesions but is atherogenic in pre-existing atherosclerosis.

OriginalsprogEngelsk
TidsskriftJACC: Basic to Translational Science
Vol/bind2
Udgave nummer5
Sider (fra-til)591-600
Antal sider10
ISSN2452-302X
DOI
StatusUdgivet - 2017

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