Metformin and kidney protection; a letter to editor on recent findings

The mechanism of metformin includes the enhancement of skeletal muscles and adipocytes glucose uptake, and inhibiting the production of glucose in liver. AMP-activated protein kinase (AMPK) via metformin, a cellular energy regulator, can be used to balance hemostasis. Treatment with metformin in glomerular mesangial cells (MCs) in a diabetic situation has resulted in the significant increase of superoxide dismutase (SOD) and malondialdehyde (MDA), monocyte chemoattractant protein-1 (MCP-1), p38 mitogen-activated protein kinase (p38MAPK) expression, the expression of nuclear factor-κB (NF-κB), intracellular p22phox mRNA and protein level, intercellular adhesion molecule-1 (ICAM-1), proinflammatory cytokines, transforming growth factor-beta 1 (TGF-β1) and ROS production suppression and lipid peroxidation. Metformin also has a reno-protective mechanism, i.e., restoring mitochondrial function integrity.