Anti-inflammatory and antiatherogenic effects of insulin

Recent clinical and experimental studies have shown that chronic vascular inflammation is an important contributor to the development of atherosclerosis. Glucose is one of several stimuli that induce cellular and molecular mechanisms of inflammation. Elevated plasma glucose concentrations have been associated with increased risk of cardiovascular disease in patients with and without diabetes. Conversely, insulin produces a number of anti-inflammatory effects. Infusion of insulin reduces the production of reactive oxygen species (ROS) by mononuclear cells in obese but otherwise healthy individuals. Insulin suppresses the activity of nuclear factor (NF)-KB (NF-KB), a transcription factor for many inflammatory cytokines. It also reduces the production of tissue-damaging matrix metalloproteinases (MMPs) and of proteins like tissue factor that stimulate thrombosis. In patients receiving fibrinolytic therapy for acute myocardial infarction (AMI), infusion of insulin for 48 hours reduces several biochemical markers of inflammation and myocardial injury. Insulin may be a valuable adjunct to current therapies for AMI. Additional clinical research is needed to identify the optimal dose and timing for insulin administration.