| First Author | Bedu E | Year | 2007 |
| Journal | Biochem Biophys Res Commun | Volume | 357 |
| Issue | 4 | Pages | 877-81 |
| PubMed ID | 17466944 | Mgi Jnum | J:121769 |
| Mgi Id | MGI:3711599 | Doi | 10.1016/j.bbrc.2007.04.003 |
| Citation | Bedu E, et al. (2007) Double gene deletion reveals the lack of cooperation between PPARalpha and PPARbeta in skeletal muscle. Biochem Biophys Res Commun 357(4):877-81 |
| abstractText | The peroxisome proliferator-activated receptors (PPARs) are involved in the regulation of most of the pathways linked to lipid metabolism. PPARalpha and PPARbeta isotypes are known to regulate muscle fatty acid oxidation and a reciprocal compensation of their function has been proposed. Herein, we investigated muscle contractile and metabolic phenotypes in PPARalpha-/-, PPARbeta-/-, and double PPARalpha-/- beta-/- mice. Heart and soleus muscle analyses show that the deletion of PPARalpha induces a decrease of the HAD activity (beta-oxidation) while soleus contractile phenotype remains unchanged. A PPARbeta deletion alone has no effect. However, these mild phenotypes are not due to a reciprocal compensation of PPARbeta and PPARalpha functions since double gene deletion PPARalpha-PPARbeta mostly reproduces the null PPARalpha-mediated reduced beta-oxidation, in addition to a shift from fast to slow fibers. In conclusion, PPARbeta is not required for maintaining skeletal muscle metabolic activity and does not compensate the lack of PPARalpha in PPARalpha null mice. |
