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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.
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http://dx.doi.org/10.1016/j.lfs.2018.09.006 | DOI Listing |
Life Sci
October 2018
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
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.
Adv Exp Med Biol
September 2017
Faculty of Medicine, Department of General Surgery, Gazi University, Besevler, Ankara, Turkey.
The decrease in adiponectin levels are negatively correlated with chronic subclinical inflammation markers in obesity. The hypertrophic adipocytes cause obesity-linked insulin resistance and metabolic syndrome. Furthermore, macrophage polarization is a key determinant regulating adiponectin receptor (AdipoR1/R2) expression and differential adiponectin-mediated macrophage inflammatory responses in obese individuals.
View Article and Find Full Text PDFInt J Cardiol
August 2016
Department of Biology, York University, Toronto, Canada. Electronic address:
Am J Physiol Regul Integr Comp Physiol
November 2012
Dept. of Human Health and Nutritional Sciences, Univ. of Guelph, Ontario, Canada.
High-fat (HF) diets impair skeletal muscle response to the insulin-sensitizing adipokine adiponectin (Ad) in rodents, preceding the development of insulin resistance. Skeletal muscle insulin response in HF-fed rats can be restored with chronic exercise; whether recovery of skeletal muscle Ad response is necessary for the exercise-induced recovery of insulin-stimulated glucose transport is not known. In the current study, insulin and Ad resistance were induced in rodents with 4 wk of HF feeding (HF(4); low-fat fed animals used as control).
View Article and Find Full Text PDF