title: Insulin: an endogenous cardioprotector.
abstract: This review discusses the myocardial protective property of the insulin/glucose-insulin-potassium regimen and the mechanisms involved in this beneficial action. Several recent studies suggest that insulin not only is useful to control hyperglycemia and maintain glucose homeostasis but also may have the unique property to protect the myocardium from reperfusion injury and ischemia and prevent apoptosis of myocardial cells. The insulin/glucose-insulin-potassium (GIK) regimen suppresses the production of tumor necrosis factor-alpha, interleukin-6, macrophage migration inhibitory factor and other pro-inflammatory cytokines, and free radicals; and enhances the synthesis of endothelial nitric oxide and anti-inflammatory cytokines interleukin-4 and interleukin-10. Thus, the insulin/GIK regimen brings about its cardioprotective action. This may also explain why the insulin/GIK regimen is useful in sepsis and septic shock, myocardial recovery in acute myocardial infarction, and critical illness. It is suggested that the infusion of adequate amounts of insulin to patients with acute myocardial infarction, congestive heart failure, cardiogenic shock, and critical illness preserves myocardial integrity and function and ensures rapid recovery. In view of the suppressive action of insulin on the synthesis of proinflammatory cytokines and free radicals, it is possible that the insulin/GIK regimen, when used in a timely and appropriate fashion, may also protect other tissues and organs and facilitate in the recovery of patients who are critically ill.
mesh_terms: D000818:Animals; D001786:Blood Glucose / Q000378:metabolism*; D016883:Diabetic Ketoacidosis / Q000188:drug therapy; D005947:Glucose / Q000008:administration & dosage; D006801:Humans; D006943:Hyperglycemia / Q000150:complications / Q000188:drug therapy* / Q000503:physiopathology; D007328:Insulin / Q000008:administration & dosage / Q000627:therapeutic use*; D007333:Insulin Resistance; D008263:Macrophage Migration-Inhibitory Factors / Q000378:metabolism; D009203:Myocardial Infarction / Q000150:complications / Q000188:drug therapy / Q000517:prevention & control*; D009569:Nitric Oxide / Q000378:metabolism; D011188:Potassium / Q000008:administration & dosage; D012772:Shock, Septic / Q000150:complications / Q000188:drug therapy; D014409:Tumor Necrosis Factor-alpha / Q000037:antagonists & inhibitors / Q000378:metabolism
chemical_list: D001786:Blood Glucose; D007328:Insulin; D008263:Macrophage Migration-Inhibitory Factors; D014409:Tumor Necrosis Factor-alpha; D009569:Nitric Oxide; D005947:Glucose; D011188:Potassium