Insulin in sepsis and septic shock.
NF-kappaB activation, and elevated concentrations of macrophage migration inhibitory factor (MIF), tumor necrosis factor-alpha (TNF-alpha), interleukin-1(IL-1), IL-6, free radicals, inducible nitric oxide (iNO), and stress hyperglycemia occurs in sepsis and this leads to systemic inflammatory response and myocardial depression seen in sepsis and septic shock. Conversely, insulin suppresses production of MIF, TNF-alpha, IL-1, IL-6, and free radicals, enhances endothelial NO generation, and enhances the production of anti-inflammatory cytokines IL-4, and IL-10, corrects stress hyperglycemia and improves myocardial function. This supports my earlier proposal that insulin (with or without glucose and potassium) therapy to maintain euglycemia suppresses the inflammatory response, improves myocardial function, and thus, is of benefit in acute myocardial infarction, sepsis andseptic shock.
Das
Undurti N
UN
Department of Nutrition and Surgery, SUNY Upstate Medical University Syracause, NY, USA.
D000818:Animals; D009202:Cardiomyopathies / Q000188:drug therapy; D006801:Humans; D007004:Hypoglycemic Agents / Q000627:therapeutic use*; D007328:Insulin / Q000502:physiology / Q000627:therapeutic use*; D007333:Insulin Resistance; D018805:Sepsis / Q000097:blood / Q000188:drug therapy* / Q000503:physiopathology; D012772:Shock, Septic / Q000097:blood / Q000188:drug therapy* / Q000503:physiopathology
D007004:Hypoglycemic Agents; D007328:Insulin