Insulin Resistance Related Aberrations in Cellular Function

Insulin resistance in DM is featured by the lack of both metabolic and vascular actions of insulin. The former results primarily in hyperglycemia whereas the latter renders the cells lacking important biochemical effects of insulin. The important action of insulin on the vasculature is related to its ability to promote vasodilatation, which is endothelium-dependent [147, 148]. Insulin triggers NO release enrolling PI3K/Akt/eNOS pathway [149, 150] and upregulates eNOS expression [151]. Insulin-resistance is characterized by impaired vasodilatory responses to insulin [152] and cholinergic stimuli [153, 154]. Furthermore, both metabolic and vascular effects of insulin share the same signaling pathways such as PI3K/Akt pathway [155]. Both insulin resistance and the down-regulation of the PI3K/Akt pathway in type 2 DM has been described in animals and in humans [87, 156, 157]. Insulin action in vascular cells also involves activation of mitogen-activated protein kinase (MAPK) signaling pathways [158]. In addition

Protein f Glucose

Protein f Glucose

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