Recently, it was suggested that PPARd might be efficacious for anti-arteriosclerosis or anti-diabetic therapy (Lee et al., 2003 and Kramer et al., 2005) and that GW501516 might improve hepatic steatosis in mice fed a high-fat diet via an improvement effect on insulin resistance (Tanaka et al., 2003). Hence, a PPARd agonist might also be efficacious against non-alcholic steatohepatitis. It is possible that the effects of PPARd in the liver might be similar to those of PPARa, at least on lipid metabolism, because GW501516 increased certain mRNAs (ACO, CPT-1 and peroxisomal ketothiolase) that would be expected to be up-regulated by a PPARa agonist (Ip et al., 2003). Indeed, it may be that in the liver, PPARd has very similar effects to those of PPARa.
In conclusion, bezafibrate may be effective at improving non-alcholic steatohepatitis. In addition, in the liver of a non-alcholic steatohepatitis model the effects of PPARd and of a PPARd agonist may also be effective against non-alcholic steatohepatitis. Accordingly, we suggest that bezafibrate may improve non-alcholic steatohepatitis not only via activation of PPARa but also via activation of PPARd, because bezafibrate is a PPAR pan-agonist.
Lol;... denk dat onze GFT-505 de perfecte eigenschappen hefft om NASH te genezen.