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. Author manuscript; available in PMC: 2014 Jan 29.
Published in final edited form as: J Burn Care Res. 2008 Sep-Oct;29(5):683–694. doi: 10.1097/BCR.0b013e31818481ce

Figure 2. Molecular mechanisms underlying insulin resistance following thermal injury.

Figure 2

Activation of JNK or IKK by cytokine signaling or lipid products during ER stress may lead to phosphorylation of IRS-1 at serine residues which may preclude its tyrosine phosphorylation by the insulin receptor tyrosine kinase, thus resulting in impaired PI3K/Akt signaling and insulin resistance with its associated consequences.