Exercise training protects human and rodent beta cells against endoplasmic reticulum stress and apoptosis

Autor(es):Mostrar menos -

Paula, Flavia M. M. ^[1] ; Leite, Nayara C. ^[2] ; Borck, Patricia C. ^[2] ; Freitas-Dias, Ricardo ^{[3, 2]} ; Cnop, Miriam ^{[1, 4]} ; Chacon-Mikahil, Mara P. T. ^[5] ; Cavaglieri, Claudia R. ^[5] ; Marchetti, Piero ^[6] ; Boschero, Antonio C. ^[2] ; Zoppi, Claudio C. ^[2] ; Eizirik, Decio L. ^[1]

Afiliação do(s) autor(es)

^[1] ULB, Erasmus Hosp, Ctr Diabet Res, Brussels - Belgium

^[2] Univ Campinas UNICAMP, Obes & Comorbid Res Ctr, Inst Biol, Dept Struct & Funct Biol, Campinas - Brazil

^[3] Univ Pernambuco, Dept Phys Therapy, Petrolina - Brazil

^[4] ULB, Erasmus Hosp, Div Endocrinol, Brussels - Belgium

^[5] Univ Campinas UNICAMP, Fac Phys Educ, Exercise Physiol Lab FISEX, Campinas - Brazil

^[6] Univ Pisa, Dept Clin & Expt Med, Pisa - Italy

• Tipo de documento: Artigo Científico
• Fonte: FASEB JOURNAL; v. 32, n. 3, p. 1524-1536, MAR 2018.
• Citações Web of Science: 4

Resumo

Prolonged exercise has positive metabolic effects in obese or diabetic individuals. These effects are usually ascribed to improvements in insulin sensitivity. We evaluated whether exercise also generates circulating signals that protect human and rodent beta cells against endoplasmic reticulum (ER) stress and apoptosis. For this purpose, we obtained serum from humans or mice before and after an 8 wk training period. Exposure of human islets or mouse or rat b cells to human or rodent sera, respectively, obtained from trained individuals reduced cytokine (IL-1 beta+IFN-gamma)- or chemical ER stressor-induced beta-cell ER stress and apoptosis, at least in part via activation of the transcription factor STAT3. These findings indicate that exercise training improves human and rodent beta-cell survival under diabetogenic conditions and support lifestyle interventions as a protective approach for both type 1 and 2 diabetes. (AU)

• Processo FAPESP: 15/12611-0 - Mecanismos moleculares envolvidos na disfunção e morte de células beta pancreáticas no Diabetes mellitus: estratégias para a inibição desses processos e para a recuperação da massa insular
• Beneficiário: Antonio Carlos Boschiero
• Modalidade de apoio: Auxílio à Pesquisa - Temático