Abstract
Type 2 diabetes (T2D) is one of the major public diseases which is characterized by peripheral insulin resistance (IR) and progressive pancreatic I3-cell failure. While in the past few years, some new factors, such as inflammation, oxidative stress, immune responses and other potential pathways, have been identified to play critical roles in T2D, and thereby provide novel promising targets for the treatment of T2D. Remote ischemic conditioning (RIC) is a non-invasive and convenient operation performed by transient, repeated ischemia in distant place. Nowadays, RIC has been established as a potentially powerful therapeutic tool for many diseases, especially in I/R injuries. Through activating a series of neural, humoral and immune pathways, it can release multiple protective signals, which then regulating inflammation, oxidative stress, immune response and so on. Interestingly, several recent studies have discovered that the beneficial effects of RIC on I/R injuries might be abolished by T2D, wherein the higher basal levels of inflammation and oxidative stress, dysregulation of immune system and some potential pathways secondary to hyperglycemia may play critical roles. In contrast, a higher intensity of conditioning could restore the protective effects. Based on the overlapped mechanisms RIC and T2D performs, we provide a hypothesis that RIC may also play a protective role in T2D via targeting these signaling pathways.
NSTL
Elsevier