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

Author(s)

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]

Affiliation

^[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

• Document type: Journal article
• Source: SCIENTIFIC REPORTS; v. 11, n. 1 APR 21 2021.
• Web of Science Citations: 0

Abstract

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)

• 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
• FAPESP's process: 18/15032-9 - Effect of resistance exercise training upon pancreatic beta-cell mass and function in healthy and diabetic mice
• Grantee: Gabriela Alves Bronczek
• Support Opportunities: Scholarships in Brazil - Doctorate
• FAPESP's process: 16/17102-9 - Function of myostatin in epigenetic control of pancreatic beta cells proliferation
• Grantee: José Maria Costa Júnior
• Support Opportunities: Scholarships in Brazil - Post-Doctoral