Resistance Training Improves Beta Cell Glucose Sensing and Survival in Diabetic Models

Autor(es)

Bronczek, Gabriela Alves ; Soares, Gabriela Moreira ; Marmentini, Carine ; Boschero, Antonio Carlos ; Costa-Junior, Jose Maria

• Tipo de documento: Artigo Científico
• Fonte: INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES; v. 23, n. 16, p. 17-pg., 2022-08-01.

Resumo

Resistance training increases insulin secretion and beta cell function in healthy mice. Here, we explored the effects of resistance training on beta cell glucose sensing and survival by using in vitro and in vivo diabetic models. A pancreatic beta cell line (INS-1E), incubated with serum from trained mice, displayed increased insulin secretion, which could be linked with increased expression of glucose transporter 2 (GLUT2) and glucokinase (GCK). When cells were exposed to pro-inflammatory cytokines (in vitro type 1 diabetes), trained serum preserved both insulin secretion and GCK expression, reduced expression of proteins related to apoptotic pathways, and also protected cells from cytokine-induced apoptosis. Using 8-week-old C57BL/6 mice, turned diabetic by multiple low doses of streptozotocin, we observed that resistance training increased muscle mass and fat deposition, reduced fasting and fed glycemia, and improved glucose tolerance. These findings may be explained by the increased fasting and fed insulinemia, along with increased beta cell mass and beta cell number per islet, observed in diabetic-trained mice compared to diabetic sedentary mice. In conclusion, we believe that resistance training stimulates the release of humoral factors which can turn beta cells more resistant to harmful conditions and improve their response to a glucose stimulus. (AU)

• Processo FAPESP: 13/07607-8 - CMPO - Centro Multidisciplinar de Pesquisa em Obesidade e Doenças Associadas
• Beneficiário: Licio Augusto Velloso
• Modalidade de apoio: Auxílio à Pesquisa - Centros de Pesquisa, Inovação e Difusão - CEPIDs
• Processo FAPESP: 21/04664-7 - 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: 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: 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