Glucose-induced beta cell production of IL-1beta contributes to glucotoxicity in human pancreatic islets.

By K. Maedler, P. Sergeev, F. Ris, J. Oberholzer, H. Joller-Jemelka, G. Spinas, N. Kaiser, P. Halban, M. Donath. Journal of Clinical Investigation, 2002

736 citations recorded by the source corpus.

View Paper: https://www.semanticscholar.org/paper/7ab03f1ae1ec938135c4b6c6fecb5ac8f769353c

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Citations in the corpus

• Aging and aging-related diseases: from molecular mechanisms to interventions and treatments (2022, background): “Circulating FFAs and glucose activate the TLR4-MyD 8 pathway and stimulate the production of proinflammatory factors and chemokines in β-cells, such as IL-1β, IL-6, IL-8, CCL2, and CXCL1.(278,279) IL-1β attenuates insulin secretion and stimulates the activation of resident immune cells.”
• Increased Number of Islet-Associated Macrophages in Type 2 Diabetes (2007, background): “production of IL-1β in diabetic islets (27; 28) may be a key regulator of the increased chemokine production.”
• Cytokines and chemokines: At the crossroads of cell signalling and inflammatory disease. (2014, background): “This then acts in an autocrine manner, binding the β-cell IL1R and triggering the activation of the transcription factor NFκB [70].”
• Regulation of Insulin Synthesis and Secretion and Pancreatic Beta-Cell Dysfunction in Diabetes (2012, unknown): “It also leads to increased production of IL-1β, subsequent NF-kB activation, increases in FAS, DNA fragmentation and damaged β-cell function [423, 424].”