Butyrate protects pancreatic beta cells from cytokine-induced dysfunction
| Autor: | Signe Schultz Pedersen, Nils Billestrup, Violeta Georgieva Tsonkova, Min Qiao, Michala Prause |
|---|---|
| Jazyk: | angličtina |
| Rok vydání: | 2021 |
| Předmět: |
Male
insulin secretion medicine.medical_specialty QH301-705.5 medicine.medical_treatment Interleukin-1beta Inflammation Butyrate Article Catalysis Cell Line Inorganic Chemistry Mice Downregulation and upregulation Insulin-Secreting Cells Internal medicine medicine Animals Humans Secretion Biology (General) Physical and Theoretical Chemistry Beta (finance) QD1-999 Molecular Biology Spectroscopy Chemistry Insulin Insulin secretion Organic Chemistry General Medicine butyrate beta cell cytokines Rats Computer Science Applications Beta cell Butyrates Cytokine Endocrinology Diabetes Mellitus Type 2 Gene Expression Regulation inflammation Cytokines medicine.symptom |
| Zdroj: | Prause, M, Pedersen, S S, Tsonkova, V, Qiao, M & Billestrup, N 2021, ' Butyrate protects pancreatic beta cells from cytokine-induced dysfunction ', International Journal of Molecular Sciences, vol. 22, no. 19, 10427 . https://doi.org/10.3390/ijms221910427 International Journal of Molecular Sciences, Vol 22, Iss 10427, p 10427 (2021) International Journal of Molecular Sciences Volume 22 Issue 19 |
| Popis: | Pancreatic beta cell dysfunction caused by metabolic and inflammatory stress contributes to the development of type 2 diabetes (T2D). Butyrate, produced by the gut microbiota, has shown beneficial effects on glucose metabolism in animals and humans and may directly affect beta cell function, but the mechanisms are poorly described. The aim of this study was to investigate the effect of butyrate on cytokine-induced beta cell dysfunction in vitro. Mouse islets, rat INS-1E, and human EndoC-βH1 beta cells were exposed long-term to non-cytotoxic concentrations of cytokines and/or butyrate to resemble the slow onset of inflammation in T2D. Beta cell function was assessed by glucose-stimulated insulin secretion (GSIS), gene expression by qPCR and RNA-sequencing, and proliferation by incorporation of EdU into newly synthesized DNA. Butyrate protected beta cells from cytokine-induced impairment of GSIS and insulin content in the three beta cell models. Beta cell proliferation was reduced by both cytokines and butyrate. Expressions of the beta cell specific genes Ins, MafA, and Ucn3 reduced by the cytokine IL-1β were not affected by butyrate. In contrast, butyrate upregulated the expression of secretion/transport-related genes and downregulated inflammatory genes induced by IL-1β in mouse islets. In summary, butyrate prevents pro-inflammatory cytokine-induced beta cell dysfunction. |
| Databáze: | OpenAIRE |
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