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. Author manuscript; available in PMC: 2009 Oct 1.
Published in final edited form as: Future Lipidol. 2008 Dec;3(6):637–649. doi: 10.2217/17460875.3.6.637

Figure 2. Common effects of weight loss and rosuvastatin treatment in obese mice.

Figure 2

In the aortic arch, we identified PPAR-γ as a regulator of oxidative stress and inflammation. Induction of PPAR-γ results in an increase of SOD1 that is associated with a reduction of the oxidation of LDL by decreasing reactive oxygen species. Induction of PPAR-γ is also associated with increased expression of CD36, resulting in increased uptake of oxidized LDL. The reduction of plaque-oxidized LDL results in an increased PPAR-γ expression that, through LXR, induces the expression of ABCA-1. This is crucial for the efflux of inflammatory lipids, which tend to reduce PPAR-γ expression, out of the plaque. Arrows indicate activation and flat ends indicate inhibition.

ABCA-1: ATP-binding cassette, subfamily A member 1; LXR: Liver X receptor; PPAR: Peroxisome proliferator-activated receptor; SOD: Superoxide dismutase.