New insights into insulin: The anti-inflammatory effect and its clinical relevance

Abstract

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.© 2014 Baishideng Publishing Group Co., Limited. All rights reserved. Key words: Insulin; Inflammation; HyperglycemiaCore 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.Sun Q, Li J, Gao F. New insights into insulin: The antiinflammatory effect and its clinical relevance. World J Diabetes 2014; 5(2): 89-96 Available from:

Assessment of platelets morphological changes and serum butyrylcholinesterase activity in children with diabetic ketoacidosis: a case control study

“…In our study, no significant difference was found between the non-DKA and the control groups regarding serum BChE activity ( p  > 0.05), while a previous study reported a significant difference between them [21]. The insignificant difference in our results may be due to the regular insulin therapy and good glycemic control of the non DKA group which inhibited inflammation and reduced oxidative stress [28, 29]. …”

“…During DKA management, receiving insulin and fluid therapy abolishes the cascade of releasing inflammatory mediators and cytokines, which in turn inhibits platelet activation and increase serum BChE activity. Insulin therapy inhibits hyperglycemia, thus attenuates glucose-mediated inflammation, which suppresses pro-inflammatory cytokines and induces anti-inflammatory mediators [28]. Correction of dehydration and hypoperfusion by fluid therapy, reduces lactic acidosis which in turn decreases inflammatory mediators release [2].…”

Anti-inflammatory Agents in the Treatment of Diabetes and Its Vascular Complications

“…Several studies have suggested that insulin may exert an anti-inflammatory response, independent of its effects on glycemia (76,77). Insulin has been shown to alleviate inflammation through several mechanisms, including increased endothelial nitric oxide release and decreased expression of proinflammatory cytokines and immune mediators, such as NF-kB, intracellular adhesion molecule-1, and MCP-1, as well as several TLRs (76).…”

“…Insulin has been shown to alleviate inflammation through several mechanisms, including increased endothelial nitric oxide release and decreased expression of proinflammatory cytokines and immune mediators, such as NF-kB, intracellular adhesion molecule-1, and MCP-1, as well as several TLRs (76). In a randomized parallel-group study in patients with type 2 diabetes, serum concentrations of hs-CRP and IL-6 were markedly reduced in insulin-treated patients compared with metformin, despite similar glycemic control (78).…”

Inflammation and Brain Aging

“…Дизре-гуляция глюкозных транспортеров GLUT 4 и GLUT 8, преимущественно в гиппокампе и миндалине головного мозга, характерна для нейровоспаления. HMGB 1 белки предложены в качестве биомаркеров метаболического синдрома, сопровождающегося развитием инсулинорези-стентности [64]. Реализация TLR4-зависимого механиз-ма врожденного иммунитета способствует проявлению инсулинорезистентности.…”