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Malatt C, Wu T, Bresee C, Hogg E, Wetheimer J, Tan E, et al
Key Points The glucose-lowering, insulin-sensitizing agent metformin works mainly by reducing gluconeogenesis and opposing glucagon-mediated signalling in the liver and, to a lesser extent, by increasing glucose uptake in skeletal muscle The primary site of metformin action is the mitochondrion The antihyperglycaemic effect of metformin is probably owing to defective protein kinase A signalling Metformin affects lipid metabolism primarily via 5-AMP-activated protein kinase (AMPK) activation Antitumourigenic effects of metformin, which require further study, might be partially due to systemic metabolic alterations, including the reduced availability of insulin In cancer cells, metformin acts as an inducer of energetic stress
The nanomaterial LA-PEG-CeNPs combines the mitochondrial targeting property of lipoic acid and the antioxidant activity of cerium nanoparticles [381]
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