Please use this identifier to cite or link to this item: http://repositorio.unicamp.br/jspui/handle/REPOSIP/242372
Type: Artigo
Title: Exercise increases pancreatic beta-cell viability in a model of type 1 diabetes through IL-6 signaling
Author: Paula, Flavia M. M.
Leite, Nayara C.
Vanzela, Emerielle C.
Kurauti, Mirian A.
Freitas-Dias, Ricardo
Carneiro, Everardo M.
Boschero, Antonio C.
Zoppi, Claudio C.
Abstract: Type 1 diabetes (T1D) is provoked by an autoimmune assault against pancreatic cells. Exercise training enhances beta cell mass in T1D. Here, we investigated how exercise signals beta 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-1 beta plus IFN-gamma). Islets from control mice and beta-cell lines (INS-1E and MIN6) were incubated with serum from control or trained mice or medium obtained from 5-aminoimidazole-4 carboxamide1-beta-D-ribofuranoside (AICAR)-treated C2C12 skeletal muscle cells. Subsequently, islets and beta cells were exposed to IL-1 beta plus IFN-gamma. Proteins were assessed by immunoblotting, apoptosis was determined by DNA-binding dye propidium iodide fluorescence, and NO center dot was estimated by nitrite. Exercise reduced 25, 75, and 50% of the IL-1 beta plus IFN-gamma-induced iNOS, nitrite, and cleaved caspase-3 content, respectively, in pancreatic islets. Serum from trained mice and medium from AICAR-treated C2C12 cells reduced beta-cell death, induced by IL-1 beta plus IFN-gamma 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 beta-cell survival in T1D through IL-6.
Type 1 diabetes (T1D) is provoked by an autoimmune assault against pancreatic cells. Exercise training enhances beta cell mass in T1D. Here, we investigated how exercise signals beta 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-1 beta plus IFN-gamma). Islets from control mice and beta-cell lines (INS-1E and MIN6) were incubated with serum from control or trained mice or medium obtained from 5-aminoimidazole-4 carboxamide1-beta-D-ribofuranoside (AICAR)-treated C2C12 skeletal muscle cells. Subsequently, islets and beta cells were exposed to IL-1 beta plus IFN-gamma. Proteins were assessed by immunoblotting, apoptosis was determined by DNA-binding dye propidium iodide fluorescence, and NO center dot was estimated by nitrite. Exercise reduced 25, 75, and 50% of the IL-1 beta plus IFN-gamma-induced iNOS, nitrite, and cleaved caspase-3 content, respectively, in pancreatic islets. Serum from trained mice and medium from AICAR-treated C2C12 cells reduced beta-cell death, induced by IL-1 beta plus IFN-gamma 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 beta-cell survival in T1D through IL-6
Subject: Exercícios físicos
Células secretoras de insulina
Ilhotas pancreáticas
Diabetes Mellitus tipo 1
Transdução de sinal
Country: Estados Unidos
Editor: Federation of American Societies for Experimental Biology
Citation: Exercise Increases Pancreatic Beta-cell Viability In A Model Of Type 1 Diabetes Through Il-6 Signaling. Federation Amer Soc Exp Biol, v. 29, p. 1805-1816 MAY-2015.
Rights: fechado
Identifier DOI: 10.1096/fj.14-264820
Address: http://www.fasebj.org/content/29/5/1805
Date Issue: 2015
Appears in Collections:IB - Artigos e Outros Documentos

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