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
  • Christoffersen, Christina
  • 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.

TidsskriftJACC: Basic to Translational Science
Udgave nummer5
Sider (fra-til)591-600
Antal sider10
StatusUdgivet - 2017

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