Symposium 17: Beta cell response to inflammation
DOI:
https://doi.org/10.47196/diab.v54i3Sup.333Keywords:
beta cell, diabetes mellitusAbstract
Symposium 17: Beta Cell Failure
Beta cell response to inflammation
Current dogma understands the pathogenesis of diabetes, type 2 diabetes mellitus (T2DM) in particular, as insulin resistance causing beta cell exhaustion which subsequently causes hyperglycemia and then glycosuria. It has recently been proposed that insulin resistance, hyperglycemia and glycosuria would act as counterregulatory responses that prevent excessive accumulation of nutrients in tissues. If these mechanisms fail, they trigger hyperactivation of the innate immune system and its harmful effects. Inflammatory mediators of the immune system are produced by immune cells and virtually all parenchymal cells respond to these under conditions of inflammation contributing to the progressive deterioration of the beta cell and the complications of diabetes.
The susceptibility of beta cells to the cytotoxic effect mediated by inflammatory cytokines in DM1 is known. Beta cells express high levels of the IL-1β receptor, and contrary to alpha cells, they express toxic mediators such as inducible nitric oxide synthase when exposed to inflammatory cytokines (Böni-Schnetzler 2009).
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