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In animal models, AMPK activation mitigates high-fat diet-induced metabolic disorders, promoting fatty acid oxidation and glucose metabolism in obese individuals while reducing fat accumulation [66]

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In addition, glutamate can enhance the production of mtROS through opening of the mitochondrial permeability transition pore (MPTP) and trigger dissipation of the mitochondrial transmembrane potential and depletion of ATP [117, 118]