Paulo Henrique Canciglieri1, Gabriel Keine Kuga2, Vitor Rosetto Muñoz1, Rafael Calais Gaspar1, Alisson Luiz da Rocha3, Leonardo Breda1, Chadi Pellegrini Anaruma2, Luciele Guerra Minuzzi1, Adelino Sanchez Ramos da Silva3, Dennys Esper Cintra4, Leandro Pereira de Moura5, Eduardo Rochete Ropelle6, José Rodrigo Pauli7. 1. Laboratory of Molecular Biology of Exercise (LaBMEx), School of Applied Sciences, University of Campinas (UNICAMP), Limeira, SP, Brazil. 2. Post-graduate Program in Movement Sciences, São Paulo State University (UNESP), Rio Claro, SP, Brazil. 3. School of Physical Education and Sport of Ribeirao Preto, University of Sao Paulo, Ribeirao Preto, SP, Brazil. 4. Laboratory of Nutritional Genomics (LabGeN), School of Applied Sciences, University of Campinas (UNICAMP), Limeira, SP, Brazil; Laboratory of Cell Signaling, Obesity and Comorbidities Research Center (OCRC), University of Campinas, Campinas, SP, Brazil. 5. Laboratory of Molecular Biology of Exercise (LaBMEx), School of Applied Sciences, University of Campinas (UNICAMP), Limeira, SP, Brazil; Post-graduate Program in Movement Sciences, São Paulo State University (UNESP), Rio Claro, SP, Brazil; Laboratory of Cell Signaling, Obesity and Comorbidities Research Center (OCRC), University of Campinas, Campinas, SP, Brazil; CEPECE - Center of Research in Sport Sciences, School of Applied Sciences, University of Campinas (UNICAMP), Limeira, SP, Brazil. 6. Laboratory of Molecular Biology of Exercise (LaBMEx), School of Applied Sciences, University of Campinas (UNICAMP), Limeira, SP, Brazil; Laboratory of Cell Signaling, Obesity and Comorbidities Research Center (OCRC), University of Campinas, Campinas, SP, Brazil; CEPECE - Center of Research in Sport Sciences, School of Applied Sciences, University of Campinas (UNICAMP), Limeira, SP, Brazil. 7. Laboratory of Molecular Biology of Exercise (LaBMEx), School of Applied Sciences, University of Campinas (UNICAMP), Limeira, SP, Brazil; Laboratory of Cell Signaling, Obesity and Comorbidities Research Center (OCRC), University of Campinas, Campinas, SP, Brazil; CEPECE - Center of Research in Sport Sciences, School of Applied Sciences, University of Campinas (UNICAMP), Limeira, SP, Brazil. Electronic address: jose.pauli@fca.unicamp.br.
Abstract
AIMS: The aim of this study was to evaluate the effects of aging on intracellular adiponectin signaling and the possible therapeutic effect of physical exercise. MAIN METHODS: Fischer 344 rats were distributed in the following groups: Young (3 months old); Sedentary Old (Old, 27 months old); and Old Exercised (Old-Exe, 27 months old), which were subjected to a short-term exercise training protocol. KEY FINDINGS: The results showed that the old rats presented glucose intolerance without increased adiposity. However, short-term exercise training reversed this disorder, which was associated with a decrease in the pleckstrin homology domain, phosphotyrosine-binding domain, and leucine zipper motif (APPL) isoform 2 (APPL2) content. The APPL isoform 1 (APPL1) and TRB3 (Tribbles homolog 3) contents were not altered. Akt phosphorylation was only increased in the old exercised rats. There was a reduction in the content of adiponectin receptor 1 in the old rats. SIGNIFICANCE: The short-term exercise training protocol was able to decrease APPL2 content in the skeletal muscle, which was accompanied by an improvement in the glucose tolerance of the old Fischer 344 rats. These findings provide new evidence supporting the role of physical exercise as a non-pharmacological therapeutic intervention to attenuate age-related deficits.
AIMS: The aim of this study was to evaluate the effects of aging on intracellular adiponectin signaling and the possible therapeutic effect of physical exercise. MAIN METHODS: Fischer 344 rats were distributed in the following groups: Young (3 months old); Sedentary Old (Old, 27 months old); and Old Exercised (Old-Exe, 27 months old), which were subjected to a short-term exercise training protocol. KEY FINDINGS: The results showed that the old rats presented glucose intolerance without increased adiposity. However, short-term exercise training reversed this disorder, which was associated with a decrease in the pleckstrin homology domain, phosphotyrosine-binding domain, and leucine zipper motif (APPL) isoform 2 (APPL2) content. The APPL isoform 1 (APPL1) and TRB3 (Tribbles homolog 3) contents were not altered. Akt phosphorylation was only increased in the old exercised rats. There was a reduction in the content of adiponectin receptor 1 in the old rats. SIGNIFICANCE: The short-term exercise training protocol was able to decrease APPL2 content in the skeletal muscle, which was accompanied by an improvement in the glucose tolerance of the old Fischer 344 rats. These findings provide new evidence supporting the role of physical exercise as a non-pharmacological therapeutic intervention to attenuate age-related deficits.
Authors: Rick B Vega; Bram Brouwers; Stephanie A Parsons; Natalie A Stephens; Maria F Pino; Andrew Hodges; Fanchao Yi; Gongxin Yu; Richard E Pratley; Steven R Smith; Lauren M Sparks Journal: Physiol Rep Date: 2020-06