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Increased atherosclerosis following treatment with a dual PPAR agonist in the ApoE knockout mouse.

Abstract：

OBJECTIVE:Recent reports have suggested that dual peroxisome proliferator-activated receptor (PPAR) alpha/gamma agonists are associated with adverse cardiovascular events. This study aimed to investigate the actions of the non-thiazolidinedione PPARalpha/gamma agonist, compound 3q, on plaque development in the apolipoprotein E knockout (apoE KO) mouse, a recognised model of accelerated plaque development. METHODS:Six-week-old male apoE KO mice were randomised to receive the dual PPARalpha/gamma agonist, compound 3q (3 mg/kg/day), the PPARgamma agonist, rosiglitazone (20 mg/kg/day), the PPARalpha agonist, gemfibrozil (100 mg/kg/day) by gavage or no treatment for 20 weeks (n=12/group). RESULTS:Gemfibrozil and rosiglitazone significantly reduced lesion area. However, compound 3q was associated with a three-fold increase in total plaque area (versus control p<0.001). This was associated with an upregulation of markers of plaque instability including vascular cell adhesion molecule-1 (3.5-fold, p<0.001), P-selectin (3.4-fold, p<0.001) monocyte chemoattractant protein-1 (3.4-fold; p<0.001) as well as the scavenger receptor, CD36 (2-fold, p<0.01). These disparate effects were observed with the dual PPAR agonist despite lowering LDL cholesterol and improving insulin sensitivity to a similar extent to PPARalpha and gamma agonists used individually. CONCLUSION:The finding of increased atherogenesis following a dual PPARalpha/gamma agonist is consistent with recent clinical findings. These data provide an important framework for further exploring the potential utility and safety of combinatorial approaches.

journal_name

Atherosclerosis

journal_title

Atherosclerosis

authors

Calkin AC,Allen TJ,Lassila M,Tikellis C,Jandeleit-Dahm KA,Thomas MC

doi

10.1016/j.atherosclerosis.2006.11.021

subject

Has Abstract

pub_date

2007-11-01 00:00:00

pages

17-22

issue

1

eissn

0021-9150

issn

1879-1484

pii

S0021-9150(06)00689-7

journal_volume

195

pub_type

杂志文章

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