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(Reference retrieved automatically from Web of Science through information on FAPESP grant and its corresponding number as mentioned in the publication by the authors.)

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

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Author(s):
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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]
Total Authors: 11
Affiliation:
[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
Total Affiliations: 6
Document type: Journal article
Source: FASEB JOURNAL; v. 32, n. 3, p. 1524-1536, MAR 2018.
Web of Science Citations: 4
Abstract

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)

FAPESP's process: 15/12611-0 - Molecular mechanisms involved in pancreatic beta cell disfunction and dead in diabetes mellitus: strategies for the inhibition of these processes and restoration of the insular mass
Grantee:Antonio Carlos Boschiero
Support Opportunities: Research Projects - Thematic Grants