Research Article
HDAC Inhibition Modulates Cardiac PPARs and Fatty Acid Metabolism in Diabetic Cardiomyopathy
Figure 4
Cardiac fatty acid metabolic proteins in control, diabetes mellitus (DM), and MPT0E014-treated DM (DM + MPT0E014) rats. Representative immunoblots and average data of (a) ratio of phosphorylated 5′ adenosine monophosphate-activated protein kinase 2α (pAMPK2α) to total AMPK2α, (b) peroxisome proliferator-activated receptor- (PPAR-) γ coactivator- (PGC-) 1α, (c) phosphorylated acetyl coenzyme A carboxylase (pACC), (d) cluster of differentiation 36 (CD36), (e) diacylglycerol acyltransferase 1 (DGAT1), and (f) DGAT2 from control (), DM (), and DM + MPT0E014 () rats. Densitometry was normalized to glyceraldehyde 3-phosphate dehydrogenase (GAPDH) as an internal control.
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