Open AccessPeroxisome Proliferator–Activated Receptor-α Gene Level Differently Affects Lipid Metabolism and Inflammation in Apolipoprotein E2 Knock-In Mice
Author(s) -
Fanny Lalloyer,
Kristiaan Wouters,
Morgane Baron,
Sandrine Caron,
Emmanuelle Vallez,
Jonathan Vanhoutte,
Eric Baugé,
Ronit Shiri-Sverdlov,
Marten H. Hofker,
Bart Staels,
Anne Tailleux
Publication year - 2011
Publication title -
arteriosclerosis, thrombosis, and vascular biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.007
H-Index - 270
eISSN - 1524-4636
pISSN - 1079-5642
DOI - 10.1161/atvbaha.110.220525
Subject(s) - fenofibrate , peroxisome proliferator activated receptor , endocrinology , medicine , inflammation , lipid metabolism , ppar agonist , steatosis , dyslipidemia , apolipoprotein e , receptor , apolipoprotein b , nuclear receptor , biology , chemistry , cholesterol , transcription factor , diabetes mellitus , biochemistry , gene , disease
Peroxisome proliferator-activated receptor-α (PPARα) is a ligand-activated transcription factor that controls lipid metabolism and inflammation. PPARα is activated by fibrates, hypolipidemic drugs used in the treatment of dyslipidemia. Previous studies assessing the influence of PPARα agonists on atherosclerosis in mice yielded conflicting results, and the implication of PPARα therein has not been assessed. The human apolipoprotein E2 knock-in (apoE2-KI) mouse is a model of mixed dyslipidemia, atherosclerosis, and nonalcoholic steatohepatitis (NASH). The aim of this study was to analyze, using homo- and heterozygous PPARα-deficient mice, the consequences of quantitative variations of PPARα gene levels and their response to the synthetic PPARα agonist fenofibrate on NASH and atherosclerosis in apoE2-KI mice.