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Effects of aerobic exercise training on microRNA-34c* expression in heart of streptozotocin-induced diabetic rats

Grant number: 16/14848-0
Support type:Scholarships in Brazil - Master
Effective date (Start): April 01, 2017
Effective date (End): April 30, 2018
Field of knowledge:Health Sciences - Physical Education
Cooperation agreement: Coordination of Improvement of Higher Education Personnel (CAPES)
Principal Investigator:Edilamar Menezes de Oliveira
Grantee:Clara Nóbrega
Home Institution: Escola de Educação Física e Esporte (EEFE). Universidade de São Paulo (USP). São Paulo , SP, Brazil

Abstract

Diabetes mellitus (DM) is a disease related to changes in glucose metabolism, involving insulin production, secretion and uptake. This disease, which already has epidemic status, triggers a number of other disorders in the patient, such as renal failure, retinal problems, and most important cardiovascular diseases that are the leading cause of death in those patients.Considering the need to develop mechanisms to reverse the prognosis brought by this disease, aerobic exercise training (AET) has emerged as a nonpharmacologic strategy for prevention and treatment of DM. AET promote glucose control, increased insulin sensitivity, decrease in body weight and consequently lipids, improves cardiovascular function by promoting the maintenance of blood pressure (BP).However, the mechanisms by which intracellular AET stimulates these responses are not yet elucidated, bringing questions about a new class of molecules that regulate post-transcriptionally the expression of its target genes: microRNAs (miR). It is known, however, that these small and endogenous messenger RNA sequences have its expression regulated by physical training.The miR-34c* presented an exaggeratedly decreased expression in the left ventricle (LV) of healthy Wistar rats submitted to AET. Moreover, in cultured cardiomyocytes of Wistar neonate, inhibition of miR-34c* promoted a sharp increase in gene expression of KLF11, and also na increased glucose uptake. It is known that KLF11 have functions involved in the regulation of cell growth by TGF- ², control the gene of insulin, and still have its expression down-regulated in heart failure.Thus, this work has the hypothesis that the AET is able to inhibits miR- 34c * in left ventricle of diabetic rats, and that this regulation can trigger responses in physiological cardiac hypertrophy, especially in metabolic improvement of this tissue and may be the response of the mechanisms that regulates Glut-4 translocation, inducing therefore increase glucose uptake in cardiac tissue, establishing an improvement in the overall framework of MD. (AU)