Diabetes mellitus is a chronic metabolic disease characterized by inappropriate recurrent or persistent hyperglycemia.
Numerous studies have demonstrated that hyperglycemia, the most significant predictor of poor clinical outcome in diabetes mellitus patients, can directly promote an inflammatory response and oxidative stress.
Although there are various causes of DM, all eventually lead to absolute or relative insulin deficiency and death of pancreatic β-cells. Thus, insulin inevitably becomes the primary medication used to treat the disease and prevent diabetic complications in all DM patients. Interestingly, an emerging body of evidence suggests that insulin suppresses the inflammatory process, not only through preventing hyperglycemia but also by modulating key inflammatory molecules.
In this review, we discuss the findings of studies done in vitro as well as clinical trials that have demonstrated an anti-inflammatory action of insulin and that have pointed to mechanisms responsible for this effect. Further, we discuss how the anti-inflammatory action of insulin bears on our current understanding of the pathophysiology and complications of both type 1 and type 2 diabetes.