| Grant number: | 18/15032-9 |
| Support Opportunities: | Scholarships in Brazil - Doctorate |
| Start date: | August 01, 2019 |
| End date: | December 31, 2022 |
| Field of knowledge: | Biological Sciences - Physiology - Physiology of Organs and Systems |
| Principal Investigator: | Antonio Carlos Boschiero |
| Grantee: | Gabriela Alves Bronczek |
| Host Institution: | Instituto de Biologia (IB). Universidade Estadual de Campinas (UNICAMP). Campinas , SP, Brazil |
| Associated research grant: | 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, AP.TEM |
Abstract Resistance exercise presents beneficial effects upon glycemic control in diabetic patients. However, most researchers investigate the link between these effects and the adaptations in skeletal muscle. Whereas the effects of resistance exercise on pancreatic beta-cell function remains unclear. Thus, the present study intent to investigate the effects of resistance exercise training upon pancreatic beta-cell mass and function in healthy mice, as well as, in vivo and in vitro Type 1 (T1D) and Type 2 (T2D) diabetic models. We believe, that the beneficial effects observed in glycemic control induced by resistance exercise, are likely due to direct effects on beta-cell function, which can be mediated by factors secreted by skeletal muscle. Therefore, we will analyze the effects of resistance exercise training on glycemic control and beta-cell mass and function in healthy and in T1D and T2D diabetic mice models. In case of beneficial effect, we will verify if the response of pancreatic beta-cell to resistance training is linked to a cross-talk mechanism between skeletal muscle and endocrine pancreas. For this purpose, we will treat a pancreatic beta-cell line (INS-1E) with 10% of serum from control, trained or diabetic trained (T1D and T2D) mice in normal conditions or exposed to stressors, such as: inductors of endoplasmic reticulum stress and other treatments used as in vitro models of T1D and T2D. Through these protocols, we believe it will be possible to understand the impact of resistance exercise on pancreatic beta-cell function in different metabolic states and the mechanisms involved in this process. Thus, these findings may play an important role in Diabetes prevention and treatment. (AU) | |
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