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. Author manuscript; available in PMC: 2009 Jan 9.
Published in final edited form as: FEBS Lett. 2007 Nov 29;582(1):97–105. doi: 10.1016/j.febslet.2007.11.057

Figure 1. Direct interaction of insulin signaling and inflammatory pathways.

Figure 1

The insulin signaling cascade branches into two main pathways. The PI3K/AKT pathway mediates insulin action on nutrient metabolism including glucose uptake. The Ras/MAPK pathway mediates insulin’s effect on gene expression, but also interacts with the PI3K-AKT pathway to control cell growth and differentiation. Activation of the insulin receptor leads to tyrosine phosphorylation of IRS1 thereby initiating signal transduction. Stimulation of the NFκB and AP-1 Fos/Jun inflammatory pathways results in the activation of the serine kinases, Ikkb and Jnk1, which reduce the signaling ability of IRS1. Additional inflammation-related negative regulators of IRS proteins include the Socs proteins and NO, which are induced in inflammation, and promote IRS degradation. NO also reduces PI3K/Akt activity by s-nitrosylation of Akt.