Nesses ultimos meses tenho focado nos esforcos dasminhas publicacoes/estudos que estavam pendentes, dentre esses estava o meutrabalho de pos-doutorado que terminei no inicio de 2015. E nessa ultima semanative a confirmacao da publicacao desse artigo. Curiosamente obtive essa informacaoda publicacao enquanto realizava um curso sobre divulgacao cientifica, quediscutia a importancia da divulgacao da ciencia produzida nas universidadespara a sociedade. E parte desse processo da divulgacao e tornar o conhecimentoproduzido em projetos de pesquisa em publicacoes na forma de artigo. Esseestudo teve como cerne investigar mecanismos de proteolise muscular, ou seja,perda de massas muscular, em animais diabeticos.http://link.springer.com/article/10.1007%2Fs11010-016-2910-zOver the last few months Ive had focused in my manuscripts and one of them was my postdoctoral's study that I finished in 2015. Last week I received the accept email of this article. I'm so proud and glad about this article accepted.Mol Cell Biochem. 2016 Dec 20. doi: 10.1007/s11010-016-2910-z. [Epub ahead of print]Dysregulation between TRIM63/FBXO32 expression and soleus muscle wasting in diabetic rats: potential role of miR-1-3p, -29a/b-3p, and -133a/b-3p.Gerlinger-Romero F1, Yonamine CY2, Junior DC2, Esteves JV2, Machado UF2.Author informationAbstractDiabetes mellitus (DM) induces a variable degree of muscle sarcopenia, which may be related to protein degradation and to the expression of both E3 ubiquitin ligases and some specific microRNAs (miRNAs). The present study investigated the effect of diabetes and acute muscle contraction upon the TRIM63 and FBXO32 expression as well as the potential involvement of some miRNAs. Diabetes was induced by streptozotocin and studied after 30 days. Soleus muscles were harvested, stimulated to contract in vitro for twitch tension analysis (0.5 Hz), 30 min later for tetanic analysis (100 Hz), and 30 min later were frozen. TRIM63 and FBXO32 proteins were quantified by western blotting; Trim63 mRNA, Fbxo32 mRNA, miR-1-3p, miR-29a-3p, miR-29b-3p, miR-133a-3p, and miR-133b-3p were quantified by qPCR. Diabetes induced sarcopenia by decreasing (P < 0.05) muscle weight/tibia length index, maximum tetanic contraction and relaxation rates, and absolute twitch and tetanic forces (P < 0.05). Diabetes decreased (P < 0.05) the Trim63 and Fbxo32 mRNAs (30%) and respective proteins (60%), and increased (P < 0.01) the miR-29b-3p (2.5-fold). In muscle from diabetic rats, acute contractile stimulus increased TRIM63 protein, miR-1-3p, miR-29a-3p, and miR-133a/b-3p, but decreased miR-29b-3p (P < 0.05). Independent of the metabolic condition, after muscle contraction, both TRIM63 and FBXO32 proteins correlated significantly with miR-1-3p, miR-29a/b-3p, and miR-133a/b-3p. All diabetes-induced regulations were reversed by insulin treatment. Concluding, the results depict that muscle wasting in long-term insulinopenic condition may not be accompanied by increased proteolysis, pointing out the protein synthesis as an important modulator of muscle sarcopenia in DM.KEYWORDS:Acute contraction; Atrogene; Sarcopenia; Soleus; Streptozotocin O mercado dos suplementos alimentares vemaumentando sua popularidade devido a varias maneiras de divulgacao e/oupropaganda. Esse mercado prepara constantemente uma variedade de novos produtoscom misturas de suplementos com efeitos bem descritos na literatura, tais como:bcaa, whey protein, caseina, cafeina e creatina; com substancias ainda compouca evidencia cientifica. Muito desses suplementos sao anunciados paraobtencao de perda de peso, bem como ganhos de massa muscular, propagandaextremamente atraente aos diversos tipos de consumidores (Palisin, Stacy, 2005).Desta maneira existe uma grande popularidadepelos suplementos compostos, chamados