Insulin in the critically ill with focus on cytokines, reactive oxygen species, HLA-DR expression.
Insulin is essential for glucose homeostasis. Insulin/glucose-insulin-potassium (GIK) regimen suppresses the production of tumor necrosis factor-alpha (TNF-alpha), interleukins-6 (IL-6), macrophage migration inhibitory factor (MIF) and other pro-inflammatory cytokines and reactive oxygen species (ROS), enhances the synthesis of endothelial nitric oxide (eNO), and anti-inflammatory cytokines interleukins-4 (IL-4) and interleukin-10 (IL-10). In subjects who are critically ill, monocyte HLA-DR expression was significantly decreased with a concomitant increase in plasma IL-10 and IL-4 concentrations. Large increases in the plasma concentrations of TNF-alpha, IL-6, sustained increase in the expression of leukocyte CD11b/CD18, and ROS generation following surgery and infections were found to be associated with increased mortality. By virtue of its actions on pro- and anti-inflammatory cytokines and ROS, insulin may have the ability to alter HLA-DR expression in the critically ill and thus bring about its beneficial actions in sepsis/septic shock, myocardial recovery following acute myocardial infarction, improve prognosis of those who are critically ill, and suppress inflammation.
Das
Undurti N
UN
UND Life Sciences, 13800 Fairhill Road, #321, Shaker Heights, OH 44120, USA.
D016638:Critical Illness; D016207:Cytokines / Q000187:drug effects*; D003920:Diabetes Mellitus / Q000517:prevention & control; D004727:Endothelium / Q000187:drug effects; D006684:HLA-DR Antigens / Q000096:biosynthesis / Q000187:drug effects*; D006801:Humans; D006943:Hyperglycemia / Q000517:prevention & control; D007328:Insulin / Q000494:pharmacology / Q000627:therapeutic use*; D009569:Nitric Oxide; D017382:Reactive Oxygen Species
D016207:Cytokines; D006684:HLA-DR Antigens; D007328:Insulin; D017382:Reactive Oxygen Species; D009569:Nitric Oxide