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

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 Fog Bentzon, Charlotte Brandt Sørensen

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Abstract

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
Nummer5
Sider (fra-til)591-600
Antal sider10
ISSN2452-302X
DOI
StatusUdgivet - okt. 2017

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