Research Paper Volume 13, Issue 6 pp 7828—7845
Chronic metformin treatment decreases cardiac injury during ischemia-reperfusion by attenuating endoplasmic reticulum stress with improved mitochondrial function
Figure 3. Administration of metformin improved mitochondrial function in aged IFM. Compared to 3 mo., dinitrophenol (DNP) uncoupled respiration was decreased in 24 mo. SSM (A) and IFM (B) using complex I substrate, supporting that aging impairs the mitochondrial respiratory chain. Metformin feeding improved oxidative phosphorylation in 24 mo. IFM oxidizing complex I substrates (B). Metformin feeding did not affect the oxidative phosphorylation in 24 mo. SSM with complex I substrates (A). Compared to 3 mo., the calcium retention capacity (CRC) was decreased in 24 mo. IFM (D), supporting that aging sensitizes to mitochondrial permeability transition pore (MPTP) opening. Metformin feeding improved the CRC in 24 mo. IFM (D) but not in 24 mo. SSM (C), indicating that metformin feeding decreased MPTP opening in 24 mo. IFM. Mean ± SEM; * p <0.05 vs. 3 mo. vehicle. †p<0.05 vs. 24 mo. vehicle. n=13 in 3 mo. vehicle group. N=5 in 3 mo. metformin treatment group. n=10 in 24 mo. vehicle group. N=9 in 24 mo. metformin treatment group.