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These metabolic disturbances impair mitochondrial depolarization, affect ATP synthesis, enhance ROS production and promote a pro-inflammatory state, all of which drive nerve damage [70]

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PTP1B is particularly notable: it dephosphorylates InsRec and IRS proteins, is expressed in liver, skeletal muscle, and adipose tissue, and remains a candidate therapeutic target in obesity, metabolic syndrome, and T2DM [227,228,229]

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