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Fig. 3 | Nutrition & Metabolism

Fig. 3

From: Endogenous asymmetric dimethylarginine accumulation contributes to the suppression of myocardial mitochondrial biogenesis in type 2 diabetic rats

Fig. 3

Impairments of mitochondrial function and biogenesis as well as their regulation in the myocardium of T2DM rats. Myocardial ATP content was measured to reflect mitochondrial function (panel a), and mitochondrial biogenesis was evaluated by mitochondrial DNA content, which was expressed by the copy number ratio of mitochondrial genes such as cytochrome C oxidase subunit I (COX I) and nuclear genes like β-actin indirectly (panel b), the activity of mitochondrial antioxidant enzyme manganese superoxide dismutase (Mn-SOD, panel c) and the content of lipid peroxidation product malondialdehyde (MDA, panel d) were determined to estimate oxidative stress, the transcription and protein expression of peroxisome proliferator-activated receptor-γ coactivator-1α (PGC-1α) & uncoupling protein 2 (UCP2) genes were detected by RT-PCR (panel e) and Western blotting (panel f) in the myocardium of control and type 2 diabetic (T2DM) rats. Graphs in panel  b, e & f represent the quantification of COX I vs β-actin, PGC-1α and UCP2 vs GAPDH (mRNA) or β-actin (Protein), respectively. Data are expressed as mean ± S.M.E.; n = 4 ~ 5. *P < 0.05, **P < 0.01 vs Control

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