Abstract: The mass and composition of skeletal muscle are critical to its function and may be regulated by different demands such as changes in mechanical stress, injury and hormonal overload. One of these changes, atrophy, characterized by a loss of protein content, is caused by conditions such as disuse, microgravity, sepsis, cancer and more. The dependent proteolytic pathway of ubiquitin-proteasome (UPS) is considered the main mechanism of protein degradation in skeletal muscle being the ubiquitin ligases are the most diverse and governed this proteolytic system. In skeletal muscle ubiquitin ligases are the main MAFbx/atrogin-1, Murf-1 (also called atrogenes), expression is controlled by transcription factors known as FOXO. A recent study in our laboratory showed that in restrained animals, supplementation of leucine, an essential amino acid that is the beginning of its metabolism in skeletal muscle, attenuated the decrease in CSA in type I fibers, involving minimization of overexpression of atrogenes. However it is not yet known the mechanism by which expression is modulated by leucine atrogenes. Therefore this study aims to investigate the effect of leucine on expression of atrogenes involves the activation of FOXO.
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