Symposium 17: Beta cell response to inflammation

Authors

  • Marcelo Perone Laboratory of Immuno-Endocrinology, Diabetes and Metabolism, Translational Medicine Research Institute (IIMT), Faculty of Biomedical Sciences- Universidad Austral, National Council for Scientific and Technical Research (CONICET), Autonomous City of Buenos Aires, Argentina

DOI:

https://doi.org/10.47196/diab.v54i3Sup.333

Keywords:

beta cell, diabetes mellitus

Abstract

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).

References

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- Ghiasi SM, Dahlby T, Andersen CH, Haataja L, Petersen S, Omar-Hmeadi M, Yang M, Pihl C, Bresson SE, Khilji MS, Klindt K, Cheta O, Perone MJ, Tyrberg B, Prats C, Barg S, Tengholm A, Arvan P, Mandrup-Poulsen T, Marzec MT. The endoplasmic reticulum chaperone glucose-regulated protein 94 is essential for proinsulin handling. Diabetes 2019; 68(4):747-760.

- Blum B, Roose AN, Barrandon O, Maehr R, Arvanites AC, Davidow LS, Davis JC, Peterson QP, Rubin LL, Melton DA. Reversal of β cell de-differentiation by a small molecule inhibitor of the TGFβ pathway.Elife. 2014 Sep 16;3:e02809.

Published

2023-01-10

How to Cite

Perone, M. (2023). Symposium 17: Beta cell response to inflammation. Journal of the Argentine Society of Diabetes, 54(3Sup), 59–59. https://doi.org/10.47196/diab.v54i3Sup.333

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