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

Administration of metformin increased phosphorylation of AMPK and ACC in aged mouse hearts. (A) Shows the protocol of metformin feeding. In metformin treated groups, metformin (300 mg/kg/day body weight) was dissolved in drinking water with sucrose (0.2g/100 ml) as sweetener and fed to mice for 2 weeks. In vehicle treated groups, mice were fed with drinking water with added sucrose (0.2g/100 ml). Compared to vehicle, metformin treatment increased the phosphorylation of AMPK and ACC in aged hearts, supporting that metformin feeding activates the AMPK in the aged hearts (B). The phosphorylation of protein S6 was increased with age, indicating an increased activity of mTORC1 (C). Metformin treatment decreased the age induced S6 phosphorylation (D). Mean ± SEM. *p

Figure 1. Administration of metformin increased phosphorylation of AMPK and ACC in aged mouse hearts. (A) Shows the protocol of metformin feeding. In metformin treated groups, metformin (300 mg/kg/day body weight) was dissolved in drinking water with sucrose (0.2g/100 ml) as sweetener and fed to mice for 2 weeks. In vehicle treated groups, mice were fed with drinking water with added sucrose (0.2g/100 ml). Compared to vehicle, metformin treatment increased the phosphorylation of AMPK and ACC in aged hearts, supporting that metformin feeding activates the AMPK in the aged hearts (B). The phosphorylation of protein S6 was increased with age, indicating an increased activity of mTORC1 (C). Metformin treatment decreased the age induced S6 phosphorylation (D). Mean ± SEM. *p<0.05 vs. vehicle, †p<0.05 vs. 3 mo.