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For instance, copper is required for the activation of MEK1 kinase, and disruption of this copper-dependent signaling contributes directly to myofibrillar disorganization and pathological hypertrophy [182, 183]

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Puerarin protects against high-fat high-sucrose diet-induced non-alcoholic fatty liver disease by modulating PARP-1/PI3K/AKT signaling pathway and facilitating mitochondrial homeostasis

The association of thiazolidinedione and metformin is very rational and very effective because metformin inhibits hepatic glucose production (improving insulin sensibility in the liver), whereas thiazolidinediones act by improving peripheral uptake and utilization of glucose in muscle and fat