Conversely, the activation of AMPK by treatment with the pro-longevity diabetes drug metformin (Met) (50 mg/kg/day for 2 wk, intraperitoneal [IP]) significantly reduced blood glucose levels ( Fig 4H and S2C Fig ), induced Egr1 expression in primary rat cardiomyocytes ( Fig 4I and S2B Fig ), and caused a nonsignificant trend for the protection of mice against DXR toxicity ( Fig 4J ).
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Fasting regulates EGR1 and protects from glucose- and dexamethasone-dependent sensitization to chemotherapy.
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