Pulmonary Hypertension in Obese Mice Is Accompanied by a Reduction in PPAR-γ Expression in Pulmonary Artery

Figure 1. (A) Representative graphics of body weight in CTL mice (CTL, n = 8) and HFD mice fed (HFD n = 10). (B) kITT (CTL n = 5 and HFD n = 5). (C) Curve and AUC during the GTT (CTL n = 5 and HFD n = 7). (D) Fasting blood glucose (CTL n = 5 and HFD n = 5). (E) Fasting serum insulin (CTL n = 5 and HFD n = 5). (F) HOMA-IR calculated from the fasting concentrations of glucose (mg/dl) and insulin (mU/L) (CTL n = 5 and HFD n = 5). (G) Adiponectin levels (CTL n = 5 and HFD n = 9). Values represent mean ± SD. **p < 0.01 vs. CTL; ***p < 0.001 vs. CTL.

Figure 2. (A) Representative images and quantification graphics (B) of PAT, ET, and PAT/ET ratio obtained by RV outflow pulsed-wave Doppler echocardiography from CTL mice (CTL, n = 12) and HFD mice (HFD n = 15). (C) RVSP obtained by catheterization from CTL mice (n = 5) and HFD mice (n = 6). (D) Correlation of RVSP/HOMA-IR in HFD mice (n = 6). (E) Correlation of RVSP/adiponectin in HFD mice (n = 6). Values represent mean ± SD. *p < 0.05 vs. CTL, **p < 0.01 vs. CTL.

Figure 3. Representative graphics of ER stress markers relative gene expression, (A) ATF6, (B) IRE1, (C) CHOP, (D) PERK, and (E) eIF2α of the pulmonary artery from CTL mice (n = 5) and HFD mice (n = 5). (F) Protein amount of phosphorylated JNK protein of the pulmonary artery from CTL mice (n = 4) and HFD mice (n = 4). Values represent mean ± SD. *p < 0.05 vs. respective CTL.

Figure 4. (A) Representative Western blots of PPARγ and β-tubulin from the pulmonary artery in CTL mice (n = 4) after 1, 2, or 4 months of HFD (n = 4). (B) Representative graphics of relative gene expression of PPAR-γ and of (C) PPAR-γ protein amount and (D) of relative gene expression of adiponectin from the pulmonary artery from CTL mice (n = 5) and HFD mice (n = 5). Values represent mean ± SD. *p < 0.05 vs. respective CTL.

Figure 5. (A) Fasting blood glucose, (B) curve and AUC during the GTT, and (C) kITT from CTL mice (n = 5), HFD mice (n = 6), HFD mice treated with PIO (n = 5), and HFD mice treated with PBA (n = 5). (D) Western blot of phosphorylated Akt protein with or without insulin stimulation in liver, adipose tissue, and skeletal muscle from CTL mice (n = 4), HFD mice (n = 4), HFD mice treated with PIO (n = 4), and HFD mice treated with PBA (n = 4). (E) Western blot of phosphorylated Akt protein with or without insulin stimulation in the pulmonary artery from CTL mice (n = 4), HFD mice (n = 4), HFD mice treated with PIO (n = 4), and HFD mice treated with PBA (n = 4). Values represent mean ± SD. *p < 0.05 vs. same group without insulin, **p < 0.01 vs. CTL, #p < 0.05 vs. HFD.

Figure 6. (A) Western blot of PPAR-γ in the pulmonary artery from CTL mice (n = 4), HFD mice (n = 4), HFD mice treated with PIO for 30 days (n = 4). (B) Circulating adiponectin levels from CTL mice (n = 4), HFD mice (n = 4), HFD mice treated with PIO for 30 days (n = 4), and HFD mice treated with PBA for 30 days (n = 4), (C) RVSP obtained by catheterization, and of PAT, ET, and PAT/ET ratio obtained by RV outflow pulsed-wave Doppler echocardiography from CTL mice (CTL, n = 6), HFD mice (n = 6), HFD mice treated with PIO for 30 days (n = 6), and HFD mice treated with PBA for 30 days (n = 5). (D) Quantification graphics of PAT, ET, and PAT/ET ratio obtained by RV outflow pulsed-wave Doppler echocardiography from CTL mice (n = 5) and HFD mice (HFD n = 5), HFD mice treated with PIO for 30 days (n = 5), and HFD mice treated with PBA for 30 days (n = 5). Values represent mean ± SD. *p < 0.001 vs. CTL, ***p < 0.001 vs. CTL and #p < 0.05 vs. HFD.