title: Is insulin an antiinflammatory molecule?
abstract: I suggest that insulin suppresses the secretion and antagonizes the harmful effects of tumor necrosis factor-alpha, macrophage migration-inhibitory factor, and superoxide anion. Therefore, the glucose-insulin-potassium regimen might be beneficial in acute myocardial infarction and useful in the management of patients with septicemia, septic shock, and other inflammatory diseases in which tumor necrosis factor-alpha and macrophage migration-inhibitory factor have important roles.
authors.affiliation: From EFA Sciences LLC, Norwood, Massachusetts, USA. undurti@hotmail.com
authors.forename: U N
authors.initials: UN
authors.lastname: Das
mesh_terms: D016883:Diabetic Ketoacidosis / Q000150:complications / Q000188:drug therapy* / Q000503:physiopathology; D005228:Fatty Acids, Essential / Q000378:metabolism; D005947:Glucose / Q000627:therapeutic use*; D006801:Humans; D007328:Insulin / Q000008:administration & dosage* / Q000627:therapeutic use*; D007333:Insulin Resistance / Q000502:physiology; D008263:Macrophage Migration-Inhibitory Factors / Q000009:adverse effects / Q000037:antagonists & inhibitors / Q000378:metabolism; D008954:Models, Biological; D009203:Myocardial Infarction / Q000188:drug therapy / Q000503:physiopathology; D011188:Potassium / Q000627:therapeutic use*; D018805:Sepsis / Q000188:drug therapy / Q000503:physiopathology; D012772:Shock, Septic / Q000188:drug therapy / Q000503:physiopathology; D013481:Superoxides / Q000009:adverse effects / Q000037:antagonists & inhibitors / Q000378:metabolism; D014409:Tumor Necrosis Factor-alpha / Q000009:adverse effects / Q000037:antagonists & inhibitors / Q000378:metabolism
chemical_list: D005228:Fatty Acids, Essential; D007328:Insulin; D008263:Macrophage Migration-Inhibitory Factors; D014409:Tumor Necrosis Factor-alpha; C030396:glucose-insulin-potassium cardioplegic solution; D013481:Superoxides; D005947:Glucose; D011188:Potassium