Published online Apr 15, 2014. doi: 10.4239/wjd.v5.i2.89
Revised: February 8, 2014
Accepted: March 3, 2014
Published online: April 15, 2014
Processing time: 140 Days and 13.6 Hours
Hyperglycemia, a commonly exhibited metabolic disorder in critically ill patients, activates the body’s inflammatory defense mechanism, causing the waterfall release of numerous inflammatory mediators and cytokines, and eventually leads to organ damage. As the only glucose-lowering hormone in the body, insulin not only alleviates the detrimental effects of hyperglycemia through its metabolic regulation, but also directly modulates inflammatory mediators and acts upon immune cells to enhance immunocompetence. In this sense, hyperglycemia is pro-inflammatory whereas insulin is anti-inflammatory. Therefore, during the past 50 years, insulin has not only been used in the treatment of diabetes, but has also been put into practical use in dealing with cardiovascular diseases and critical illnesses. This review summarizes the recent advances regarding the anti-inflammatory effects of insulin in both basic research and clinical trials, with the hope of aiding in the design of further experimental research and promoting effective insulin administration in clinical practice.
Core tip: Hyperglycemia is closely correlated with poor outcomes of morbidity and mortality in critically ill patients. As the only glucose-lowering hormone in the body, insulin not only alleviates the detrimental effects of hyperglycemia through its metabolic regulation, but also directly modulates inflammatory mediators and acts upon immune cells to enhance immunocompetence. This review summarizes the recent advances regarding the anti-inflammatory effects of insulin from our laboratory as well as others, in the hope of leading to a better understanding of this old, classic and wonder hormone and its wider and effective applications in clinical practice.