Cardiomyocyte-Restricted Deletion of PPARβ/δ in PPARα-Null Mice Causes Impaired Mitochondrial Biogenesis and Defense, but No Further Depression of Myocardial Fatty Acid Oxidation
Figure 3
Expression of key proteins in fatty acid and glucose metabolism. (a) Real-time PCR results for transcript expression of PPARα, PPARβ/δ, and PPARγ on RNA samples extracted from ventricular tissues of TMCM, PPARα −/−, TMPD, and TMPDPA mice. (b) Western blotting results of PPARβ/δ protein levels in nuclear proteins from ventricular tissues of TMCM, PPARα −/−, TMPD, and TMPDPA mice. (c) Transcript level of fatty acid metabolism genes in samples from ventricular tissues of TMCM, PPARα −/−, TMPD, and TMPDPA mice. Expressions of CD36, ACADM, ACADL, MCD, CPT1b, CPTII, UCP2, and FABP are shown. (d) Protein levels of FABP and CPT-Ib in samples from ventricular tissues of TMCM, PPARα −/−, TMPD, and TMPDPA mice. (e) Transcript levels of Glut1, Glut4, HK2, and PFKII in samples from ventricular tissues of TMCM, PPARα −/−, TMPD, and TMPDPA mice. (f) Protein levels of Glut1 and Glut4 in samples from ventricular tissues of TMCM, PPARα −/−, TMPD, and TMPDPA mice. versus TMCM; versus TMCM.
