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First, mitochondrial dysfunction and metabolic abnormalities may act as potential initiating factors in PEM, manifesting as impaired ATP synthesis, overproduction of reactive oxygen species (ROS), and the accumulation of metabolic byproducts

These effects were linked to the activation of signaling pathways such as FAK-paxillin, suggesting a role in regulating cellular movement and structural organization in experimental systems

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It is also possible for insulin to reach the skeletal muscle cells via paracellular transport but this mechanism is likely to be limiting due to the fact that the capillaries of muscle tissue possess a single layer of endothelial cells connected by tight junctions