Exercise increases pancreatic β‐cell viability in a model of type 1 diabetes through IL‐6 signaling
Autor: | Flavia M.M. Paula, Nayara C. Leite, Mirian Ayumi Kurauti, Cláudio Cesar Zoppi, Ricardo Freitas-Dias, Emerielle C. Vanzela, Everardo M. Carneiro, Antonio C. Boschero |
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Rok vydání: | 2015 |
Předmět: |
Male
medicine.medical_specialty Blotting Western Interleukin-1beta Radioimmunoassay Apoptosis Nitric Oxide Real-Time Polymerase Chain Reaction Biochemistry Nitric oxide Proinflammatory cytokine Interferon-gamma Islets of Langerhans Mice chemistry.chemical_compound Insulin-Secreting Cells Physical Conditioning Animal Internal medicine Genetics medicine Animals Insulin Interferon gamma RNA Messenger Viability assay Propidium iodide Muscle Skeletal Molecular Biology Cells Cultured Cell Proliferation Mice Knockout Interleukin-6 Reverse Transcriptase Polymerase Chain Reaction Chemistry Pancreatic islets Skeletal muscle Mice Inbred C57BL Diabetes Mellitus Type 1 Glucose Endocrinology medicine.anatomical_structure Signal Transduction Biotechnology medicine.drug |
Zdroj: | The FASEB Journal. 29:1805-1816 |
ISSN: | 1530-6860 0892-6638 |
Popis: | Type 1 diabetes (T1D) is provoked by an autoimmune assault against pancreatic β cells. Exercise training enhances β-cell mass in T1D. Here, we investigated how exercise signals β cells in T1D condition. For this, we used several approaches. Wild-type and IL-6 knockout (KO) C57BL/6 mice were exercised. Afterward, islets from control and trained mice were exposed to inflammatory cytokines (IL-1β plus IFN-γ). Islets from control mice and β-cell lines (INS-1E and MIN6) were incubated with serum from control or trained mice or medium obtained from 5-aminoimidazole-4 carboxamide1-β-d-ribofuranoside (AICAR)-treated C2C12 skeletal muscle cells. Subsequently, islets and β cells were exposed to IL-1β plus IFN-γ. Proteins were assessed by immunoblotting, apoptosis was determined by DNA-binding dye propidium iodide fluorescence, and NO(•) was estimated by nitrite. Exercise reduced 25, 75, and 50% of the IL-1β plus IFN-γ-induced iNOS, nitrite, and cleaved caspase-3 content, respectively, in pancreatic islets. Serum from trained mice and medium from AICAR-treated C2C12 cells reduced β-cell death, induced by IL-1β plus IFN-γ treatment, in 15 and 38%, respectively. This effect was lost in samples treated with IL-6 inhibitor or with serum from exercised IL-6 KO mice. In conclusion, muscle contraction signals β-cell survival in T1D through IL-6. |
Databáze: | OpenAIRE |
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