کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
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1937948 | 1050729 | 2007 | 5 صفحه PDF | دانلود رایگان |
The peroxisome proliferator-activated receptors (PPARs) are involved in the regulation of most of the pathways linked to lipid metabolism. PPARα and PPARβ 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 PPARα−/−, PPARβ−/−, and double PPARα−/− β−/− mice. Heart and soleus muscle analyses show that the deletion of PPARα induces a decrease of the HAD activity (β-oxidation) while soleus contractile phenotype remains unchanged. A PPARβ deletion alone has no effect. However, these mild phenotypes are not due to a reciprocal compensation of PPARβ and PPARα functions since double gene deletion PPARα–PPARβ mostly reproduces the null PPARα-mediated reduced β-oxidation, in addition to a shift from fast to slow fibers. In conclusion, PPARβ is not required for maintaining skeletal muscle metabolic activity and does not compensate the lack of PPARα in PPARα null mice.
Journal: Biochemical and Biophysical Research Communications - Volume 357, Issue 4, 15 June 2007, Pages 877–881