Resistance exercise training improves glucose homeostasis by enhancing insulin secretion in C57BL/6 mice

Autor(es)

Bronczek, Gabriela Alves ^[1] ; Soares, Gabriela Moreira ^[1] ; de Barros, Jaqueline Fernandes ^[1] ; Vettorazzi, Jean Franciesco ^[2] ; Kurauti, Mirian Ayumi ^[3] ; Marconato-Junior, Emilio ^[1] ; Zangerolamo, Lucas ^[1] ; Marmentini, Carine ^[1] ; Boschero, Antonio Carlos ^[1] ; Costa-Junior, Jose Maria ^[1]

Afiliação do(s) autor(es)

^[1] Univ Estadual Campinas, Inst Biol, UNICAMP, Obes & Comorbid Res Ctr, Campinas, SP - Brazil

^[2] Educ Union Cascavel UNIVEL, Cascavel, Parana - Brazil

^[3] State Univ Maringa UEM, Biol Sci Ctr, Dept Physiol Sci, Maringa, Parana - Brazil

• Tipo de documento: Artigo Científico
• Fonte: SCIENTIFIC REPORTS; v. 11, n. 1 APR 21 2021.
• Citações Web of Science: 0

Resumo

Resistance exercise exerts beneficial effects on glycemic control, which could be mediated by exercise-induced humoral factors released in the bloodstream. Here, we used C57Bl/6 healthy mice, submitted to resistance exercise training for 10 weeks. Trained mice presented higher muscle weight and maximum voluntary carrying capacity, combined with reduced body weight gain and fat deposition. Resistance training improved glucose tolerance and reduced glycemia, with no alterations in insulin sensitivity. In addition, trained mice displayed higher insulinemia in fed state, associated with increased glucose-stimulated insulin secretion. Islets from trained mice showed reduced expression of genes related to endoplasmic reticulum (ER) stress, associated with increased expression of Ins2. INS-1E beta-cells incubated with serum from trained mice displayed similar pattern of insulin secretion and gene expression than isolated islets from trained mice. When exposed to CPA (an ER stress inducer), the serum from trained mice partially preserved the secretory function of INS-1E cells, and prevented CPA-induced apoptosis. These data suggest that resistance training, in healthy mice, improves glucose homeostasis by enhancing insulin secretion, which could be driven, at least in part, by humoral factors. (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
• Processo FAPESP: 18/15032-9 - Efeito do treinamento resistido sobre a função e massa das células beta pancreáticas de roedores saudáveis e diabéticos
• Beneficiário: Gabriela Alves Bronczek
• Modalidade de apoio: Bolsas no Brasil - Doutorado
• Processo FAPESP: 16/17102-9 - Função da miostatina no controle epigenético da proliferação de células beta pancreáticas
• Beneficiário: José Maria Costa Júnior
• Modalidade de apoio: Bolsas no Brasil - Pós-Doutorado