Insulin infusion in acute illness
J. Clin. Invest. Paresh Dandona, et al. 115:2069 doi:10.1172/JCI26045 [Go to this article.]

Figure 1
The antiinflammatory effect of insulin and the proinflammatory effect of glucose. Insulin suppresses ROS and O₂^– generation and NADPH oxidase expression, while glucose stimulates both. Within the macrophage, O₂^– activates inhibitor of NF-κB kinase β (IKKβ) to enhance phosphorylation of IκB (α and β) such that it undergoes proteasomal degradation, releasing NF-κB to translocate into the nucleus. NF-κB stimulates the transcription of genes encoding proinflammatory proteins including TNF-α, IL-6, monocyte chemoattractant protein 1 (MCP-1), and MMPs. Within the endothelial cell, insulin also induces eNOS expression in endothelial cells, which leads to controlled NO release and vasodilation, while glucose has the opposite effect. Glucose induces the expression of adhesion molecules ICAM-1 and E-selectin, while insulin suppresses their expression in the endothelial cell. sE-selectin, soluble E-selectin; sICAM-1, soluble ICAM-1