Document Detail


Exercise training reduces insulin resistance and upregulates the mTOR/p70S6k pathway in cardiac muscle of diet-induced obesity rats.
MedLine Citation:
PMID:  20717955     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Obesity and insulin resistance are rapidly expanding public health problems. These disturbances are related to many diseases, including heart pathology. Acting through the Akt/mTOR pathway, insulin has numerous and important physiological functions, such as the induction of growth and survival of many cell types and cardiac hypertrophy. However, obesity and insulin resistance can alter mTOR/p70S6k. Exercise training is known to induce this pathway, but never in the heart of diet-induced obesity subjects. To evaluate the effect of exercise training on mTOR/p70S6k in the heart of obese Wistar rats, we analyzed the effects of 12 weeks of swimming on obese rats, induced by a high-fat diet. Exercise training reduced epididymal fat, fasting serum insulin and plasma glucose disappearance. Western blot analyses showed that exercise training increased the ability of insulin to phosphorylate intracellular molecules such as Akt (2.3-fold) and Foxo1 (1.7-fold). Moreover, reduced activities and expressions of proteins, induced by the high-fat diet in rats, such as phospho-JNK (1.9-fold), NF-kB (1.6-fold) and PTP-1B (1.5-fold), were observed. Finally, exercise training increased the activities of the transduction pathways of insulin-dependent protein synthesis, as shown by increases in Raptor phosphorylation (1.7-fold), p70S6k phosphorylation (1.9-fold), and 4E-BP1 phosphorylation (1.4-fold) and a reduction in atrogin-1 expression (2.1-fold). Results demonstrate a pivotal regulatory role of exercise training on the Akt/mTOR pathway, in turn, promoting protein synthesis and antagonizing protein degradation.
Authors:
Cleber Medeiros; Marisa J Frederico; Gabrielle da Luz; José R Pauli; Adelino S R Silva; Ricardo A Pinho; Lício A Velloso; Eduardo R Ropelle; Cláudio T De Souza
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Journal of cellular physiology     Volume:  226     ISSN:  1097-4652     ISO Abbreviation:  J. Cell. Physiol.     Publication Date:  2011 Mar 
Date Detail:
Created Date:  2010-12-30     Completed Date:  2011-01-27     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  0050222     Medline TA:  J Cell Physiol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  666-74     Citation Subset:  IM    
Copyright Information:
Copyright © 2010 Wiley-Liss, Inc.
Affiliation:
Exercise Biochemistry and Physiology Laboratory, Postgraduate Program in Health Sciences, Health Sciences Unit, University of Southern Santa Catarina, Criciúma, SC, Brazil.
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MeSH Terms
Descriptor/Qualifier:
Animals
Dietary Fats / administration & dosage,  pharmacology
Inflammation / pathology
Insulin / metabolism,  pharmacology
Insulin Resistance*
Muscle Proteins / metabolism
Myocardium / enzymology*,  metabolism,  pathology
Obesity / enzymology*,  pathology
Physical Conditioning, Animal*
Protein Biosynthesis / drug effects
Rats
Rats, Wistar
Ribosomal Protein S6 Kinases, 70-kDa / metabolism*
SKP Cullin F-Box Protein Ligases / metabolism
Signal Transduction / drug effects
TOR Serine-Threonine Kinases / metabolism*
Up-Regulation* / drug effects
Chemical
Reg. No./Substance:
0/Dietary Fats; 0/Muscle Proteins; 11061-68-0/Insulin; EC 2.7.1.1/TOR Serine-Threonine Kinases; EC 2.7.11.1/Ribosomal Protein S6 Kinases, 70-kDa; EC 6.3.2.19/Fbxo32 protein, rat; EC 6.3.2.19/SKP Cullin F-Box Protein Ligases

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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