The DOI matches its Crossref record; 10 of the 10 references it cites were found in a registry or an index.
Free Fatty Acids Induce a Proinflammatory Response in Islets via the Abundantly Expressed Interleukin-1 Receptor I
Abstract
Islets of patients with type 2 diabetes mellitus (T2DM) display features of an inflammatory process including elevated levels of the cytokine IL-1β, various chemokines, and macrophages. IL-1β is a master regulator of inflammation, and IL-1 receptor type I (IL-1RI) blockage improves glycemia and insulin secretion in humans with T2DM and in high-fat-fed mice pointing to a pivotal role of IL-1RI activity in intra-islet inflammation. Given the association of dyslipidemia and T2DM, we tested whether free fatty acids (FFA) promote the expression of proinflammatory factors in human and mouse islets and investigated a role for the IL-1RI in this response. A comparison of 22 mouse tissues revealed the highest IL-1RI expression levels in islets and MIN6 β-cells. FFA induced IL-1β, IL-6, and IL-8 in human islets and IL-1β and KC in mouse islets. Elevated glucose concentrations enhanced FFA-induced proinflammatory factors in human islets. Blocking the IL-1RI with the IL-1R antagonist (IL-1Ra) strongly inhibited FFA-mediated expression of proinflammatory factors in human and mouse islets. Antibody inhibition of IL-1β revealed that FFA stimulated IL-1RI activity via the induction of the receptor ligand. FFA-induced IL-1β and KC expression in mouse islets was completely dependent on the IL-1R/Toll-like receptor (TLR) docking protein Myd88 and partly dependent on TLR2 and -4. Activation of TLR2 in purified human β-cells and islets stimulated the expression of proinflammatory factors, and IL-1RI activity increased the TLR2 response in human islets. We conclude that FFA and TLR stimulation induce proinflammatory factors in islets and that IL-1RI engagement results in signal amplification.
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Citations
Cites
Inflammation, stress, and diabetes
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TLR4 links innate immunity and fatty acid-induced insulin resistance
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Dinarello, C. A. (2009) · Annual Review of Immunology · doi:10.1146/annurev.immunol.021908.132612 · Cited by 3,466
Interleukin-1-receptor antagonist in type 2 diabetes mellitus
Larsen, C. M., Faulenbach, M., Vaag, A., Vølund, A., Ehses, J. A., Seifert, B., Mandrup-Poulsen, T., & Donath, M. Y. (2007) · New England Journal of Medicine · doi:10.1056/nejmoa065213 · Cited by 1,798
Self-citationLee, J. Y., Sohn, K. H., Rhee, S. H., & Hwang, D. (2001) · Journal of Biological Chemistry · doi:10.1074/jbc.m011695200 · Cited by 1,299
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Cutting Edge: TLR2 Is a Functional Receptor for Acute-Phase Serum Amyloid A
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Proliferation of sorted human and rat beta cells
Parnaud, G., Bosco, D., Berney, T., Pattou, F., Kerr-Conte, J., Donath, M. Y., Bruun, C., Mandrup-Poulsen, T., Billestrup, N., & Halban, P. A. (2007) · Diabetologia · doi:10.1007/s00125-007-0855-1 · Cited by 232
Self-citationThe Interleukin‐1 Receptor Family
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Cited by
Type 2 diabetes as an inflammatory disease
Donath, M. Y., & Shoelson, S. E. (2011) · Nature Reviews Immunology · doi:10.1038/nri2925 · Cited by 3,737
Self-citationInflammation in obesity, diabetes, and related disorders
Rohm, T. V., Meier, D. T., Olefsky, J. M., & Donath, M. Y. (2022) · Immunity · doi:10.1016/j.immuni.2021.12.013 · Cited by 2,066
Self-citationInflammation as a link between obesity, metabolic syndrome and type 2 diabetes
Esser, N., Legrand-Poels, S., Piette, J., Scheen, A. J., & Paquot, N. (2014) · Diabetes Research and Clinical Practice · doi:10.1016/j.diabres.2014.04.006 · Cited by 1,981
Pathophysiology and treatment of type 2 diabetes: perspectives on the past, present, and future
Kahn, S. E., Cooper, M. E., & Del Prato, S. (2014) · The Lancet · doi:10.1016/s0140-6736(13)62154-6 · Cited by 1,743
The Role of Inflammation in Diabetes: Current Concepts and Future Perspectives
Tsalamandris, S., Antonopoulos, A. S., Oikonomou, E., Papamikroulis, G.-A., Vogiatzi, G., Papaioannou, S., Deftereos, S., & Tousoulis, D. (2019) · European Cardiology Review · doi:10.15420/ecr.2018.33.1 · Cited by 1,381
Metadata
- Authors
- Böni-Schnetzler, M., Boller, S., Debray, S., Bouzakri, K., Meier, D. T., Prazak, R., Kerr-Conte, J., Pattou, F., Ehses, J. A., Schuit, F. C., & Donath, M. Y.
- Venue
- Endocrinology
- Publisher
- The Endocrine Society
- Published
- 2009-10-09
- Volume
- 150
- Issue
- 12
- Pages
- 5218-5229
- ISSN
- 0013-7227 (ISSN-L)
- 1945-7170
- OpenAlex
- W1990902267
- Cited by
- 339
- References
- 10
- FWCI
- 18.45
- Type
- journal article
- Language
- en
- Open access
- closed
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- Böni-Schnetzler, M., Boller, S., Debray, S., Bouzakri, K., Meier, D. T., Prazak, R., Kerr-Conte, J., Pattou, F., Ehses, J. A., Schuit, F. C., & Donath, M. Y. (2009). Free Fatty Acids Induce a Proinflammatory Response in Islets via the Abundantly Expressed Interleukin-1 Receptor I. Endocrinology. https://doi.org/10.1210/en.2009-0543
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