Symposium 17: Beta cell response to inflammation

Abstract

Symposium 17: Beta cell failure Beta cell response to inflammation The current dogma understands the pathogenesis of diabetes, especially type 2, as the resistance to insulin that causes the exhaustion of the beta-cell, which will later cause hyperglycemia and, subsequently, glycosuria. It has been recently proposed that resistance to insulin, hyperglycemia and glycosuria might act as counterregulatory responses which prevent the excessive accumulation of nutrients in the tissue. If these mechanisms fail, the hyperarousal of the innate immune system and its harmful effects will sharply increase. The inflammatory mediators of the immune system are produced by immune cells and, practically, all parenchymal cells respond to them in inflammatory conditions, contributing to the progressive damage of the beta¬ cell and to diabetes complications. The susceptibility of the beta-cell to the cytotoxic effect caused by the inflammatory cytokines in T1D is well-known. Beta-cells show high levels of receptor IL-1ß and, contrary to what happens with alpha-cells, they exhibit toxic mediators such as inducible nitric oxide synthase, when exposed to inflammatory cytokines (Böni-Schnetzler 2009).

Keywords

• célula beta
• diabetes mellitus.