Insulin Resistance: A Proinflammatory State Mediated by Lipid-Induced Signaling Dysfunction and Involved in Atherosclerotic Plaque Instability

<table><i> Lipid signaling interference generates insulin resistance</i>.   (a) Signaling through phosphatidylinositol
3-kinase (PI3-K) is crucial for insulin-mediated glucose transport in
hepatocytes and skeletal muscle cells and for inflammatory protein and hormone
secretion in adipocytes and pancreatic <i>β</i>cells. Free fatty acids (FFAs)
induce a defective insulin-mediated signaling mainly through the activation of protein
kinase C (PKC <i>θ</i>), inhibitor <i>κ</i>B kinase (IKK) and c-Jun
N-terminal kinase (JNK). (b) Main cell types involved in the
development of insulin resistance. (c) Main inflammatory cell
populations involved in hyperinsulinemia-induced inflammatory states.</table>

Mediators of Inflammation

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Figure 1

Figure 1: Insulin Resistance: A Proinflammatory State Mediated by Lipid-Induced Signaling Dysfunction and Involved in Atherosclerotic Plaque Instability 

Figure 1 | Insulin Resistance: A Proinflammatory State Mediated by Lipid-Induced Signaling Dysfunction and Involved in Atherosclerotic Plaque Instability 