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Fig. 8 | Journal of Biomedical Science

Fig. 8

From: Mechanisms of inflammatory responses and development of insulin resistance: how are they interlinked?

Fig. 8

Mechanism of oxidative stress-induced IR: Chronic exposure of hyperglycemia and hyperlipidemia due to over nutrition leads to the production of oxidative stress via activation of reactive oxygen species. Once, oxidative stress is produced within the body, it leads to the activation of various transcriptional mediated pathways such as p38, JNK, IKKβ and/or NF-κB. IKKβ also induces the activation of NF-κB. p38, JNK and IKKβ, further activates the serine phosphorylation of insulin receptor substrate-1 (IRS-1). While on the other side, NF-κB also activates the expression of iNOS which also induces the S-nitrosylation of IRS-1. Both S-nitrosylation and serine phosphorylation of IRS-1 suppress the tyrosine phosphorylation of insulin signaling pathways which ultimately results into the induction of IR in liver, adipocytes and skeletal muscles

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