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The IR usually progresses in silence and manifests clinically years after being present in the form of hyperglycemia, favoring atherogenesis and plaque progression in a curvilinear relationship with vascular disease, even in the absence of hyperglycemia ( 2 O 2 and O 2 activate stress-sensitive serine/threonine kinases such as JNK, IKK, and PKC, which phosphorylate IRS-1 at inhibitory serine residues (Ser307, Ser612), disrupting its interaction with the insulin receptor and promoting proteasomal degradation (Roden et al., 2017)

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