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Listed mechanisms include IR serine phosphorylation states, IRS-1 modifications, PI3K/AKT pathway attenuation, GLUT4 expression changes, SNARE complex assembly defects, Rab GTPase cycling alterations, AS160/Tbc1D4 dysregulation, mTORC1/mTORC2 signaling perturbations, and inflammatory mediator effects (TNF-α, SOCS3, IL-6)
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