FIG. 3.

PPARγ activation and mitochondrial function parameters in atrial myocardium. Shown in (A) are representative immunoblots of PPARγ in nuclear extracts prepared from 4 individual Ctl and n-3 PUFA-treated patients, with TATA-binding protein (TATA-BP) as nuclear protein loading control. In (B) is densitometry analysis of nuclear PPARγ in atrial tissue from both groups (N=10). Shown in (C) is expression of genes known to be activated by PPARγ. Rates of basal and maximal ADP-stimulated (5 mM) mitochondrial O₂ consumption supported by (D) palmitoyl-carnitine in both treatment groups. Data shown in (E) are rates of mitochondrial O₂ consumption supported by pyruvate+malate (PM) in the absence and presence of ADP (500 μM). In (F) are rates of mitochondrial ATP release with PM+500 μM ADP, and in (G) are ATP/O ratio in the presence of PM+500 μM ADP. Gene expression data are reported as mean±SD. Raw data are shown for mitochondrial experiments in both treatment groups, along with the mean (faint horizontal line). N=10–12 for each group, for all experiments. *p<0.05 versus Ctl, **p<0.01 versus Ctl.