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 Mikael Helweg Heegaard, Christina Christoffersen, Lars Bolund, Mette Schmidt, Ying Liu, Juan Li, Rong Li, Henrik Callesen, Jacob F. Bentzon, Charlotte B. Sørensen

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    Abstract

    Summary: 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.
    Original languageEnglish
    JournalJ A C C: Basic to Translational Science
    Volume2
    Issue number5
    Pages (from-to)591-600
    ISSN2452-302X
    DOIs
    Publication statusPublished - 2017

    Bibliographical note

    This is an open access article under the CC BY-NC-ND license.

    Keywords

    • Apolipoprotein E
    • Atherosclerosis
    • Pig
    • Remnant cholesterol dysbetalipoproteinemia

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