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The mechanisms underlying these effects include the inhibition of protein tyrosine phosphatase 1B (PTP1B), which is physiologically responsible for insulin receptor inhibition through dephosphorylation and attenuates insulin signal transduction (123, 124)

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Second, electron transport chain (ETC.) impairment involves dysfunction of complexes I-IV, leading to reduced electron transfer efficiency, decreased ATP generation, and increased electron leakage that promotes excessive reactive oxygen species (ROS) production (Li JY