Influence of resistance exercise training in diabetic hypertrophy renal: The role of mTOR and Acetyl CoA Carboxylase

Abstract

Diabetic kidney disease (DKD) is a progressive complication that develops from diabetes. An important change observed is renal hypertrophy associated with the mTOR pathway. On the other hand, increasing evidence indicates that the reduction in the phosphorylation of Acetyl‐CoA Carboxylase (ACC) may be important in the development of Renal Fibrosis. Therefore, it is fundamental to understand non‐pharmacological intervention as the effect of resistance training (RET) to prevent these complications.In this study, our aim is evaluating the RET on the renal hypertrophy.Male Wistar rats were divided into 4 groups: control (C=8), control trained (CT=8), diabetic (D=8) and diabetic trained (DT=8). DM (glycaemia>250mg/dL) was induced by Streptozotocin (STZ) (50mg/kg, i.v.). Trained groups were submitted to a resistance exercise training protocol on Ladder climb (8wk). The expression of Akt/mTOR pathway was evaluated by two technical, western blotting and multiplex. Immunohistochemical was used to analyze the expression by ACC. A hypertrophy renal index was calculated by the reason the kidney weight/body weight. The histomorphology was analyzed by hematoxylin and eosin stain.RET improved renal parameters in the DT group showing a decreased proteinuria (DS:15±1.5; DT:16±2.0; CS:38±3; CT:16±2mg/24h). The renal expression of mTOR and Akt, was increased in the DS animals, and the early RET was able to prevent, the same results were observed in the hypertrophy renal index (p<0,05). The ACC was decreased in DS group and RET normalized this expression (p<0,05). Surprisingly, when analyzing the morphology was not find any difference between the groups.Our findings showed that RET was able to prevent renal hypertrophy, molecularly, and improvement of the renal parameters induced by experimental diabetes. These results demonstrate that the RET the clinical application in early diabetic patients may help prevent and/or treat the renal hypertrophy.Support or Funding InformationSources of Funding This study was supported by Fundacao de Amparo a Pesquisa do Estado de Sao Paulo (FAPESP) and Conselho Nacional de Desenvolvimento Cientıfico e Tecnologico (CNPq).This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.