| Grant number: | 16/11661-6 |
| Support Opportunities: | Scholarships in Brazil - Scientific Initiation |
| Start date: | September 01, 2016 |
| End date: | December 31, 2017 |
| Field of knowledge: | Biological Sciences - Physiology - General Physiology |
| Principal Investigator: | Rui Curi |
| Grantee: | Maria Vitoria Martins Scervino |
| Host Institution: | Instituto de Ciências Biomédicas (ICB). Universidade de São Paulo (USP). São Paulo , SP, Brazil |
Abstract Type 1 diabetic patients present intense loss of force and skeletal muscle mass. Skeletal muscle from diabetic rats submitted to hypertrophy by functional overload, shows increased muscle size at the same magnitude as control animals. However, under diabetic and other catabolic states a significant increase in skeletal muscle autophagy is observed. Autophagy is an important self-degradating process to mantain cellular homeostasis and also regulates skeletal muscle mass. The experiments will be performed in muscles with predominance of glycolytic (long digital extensor - EDL) and oxidative (soleus) fibers. In this study, we will evaluate proteins markers of autophagy during skeletal muscle hypertrophy induced by functional overload in streptozotocin induced diabetic rats. Autophagy process will be evaluated at seven day-period after overload-induced hypertrophy in EDL and soleus muscles through muscle tibialis anterior synergistic ablation and tenotomy of gastrocnemius muscle, respectively. During this period, protein synthesis pathway reaches the maximal activity. Molecular markers associated to autophagy pathway in skeletal muscle, to be assessed by western blotting, are involved in the autolisosome formation and maturation processes: LC3, Beclin1, Atg7, p62, p-ULK1 ULK1. | |
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