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Overload-induced skeletal muscle hypertrophy is not impaired in STZ-diabetic rats
The aim of this study was to evaluate the effect of overload-induced hypertrophy on extensor digitorum longus (EDL) and soleus muscles of streptozotocin-induced diabetic rats. The overload-induced hypertrophy and absolute tetanic and twitch forces increases in EDL and soleus muscles were not differe...
Autores principales: | , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
John Wiley & Sons, Ltd
2015
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4552534/ https://www.ncbi.nlm.nih.gov/pubmed/26197932 http://dx.doi.org/10.14814/phy2.12457 |
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author | Fortes, Marco Aurélio S Pinheiro, Carlos Hermano J Guimarães-Ferreira, Lucas Vitzel, Kaio F Vasconcelos, Diogo A A Curi, Rui |
author_facet | Fortes, Marco Aurélio S Pinheiro, Carlos Hermano J Guimarães-Ferreira, Lucas Vitzel, Kaio F Vasconcelos, Diogo A A Curi, Rui |
author_sort | Fortes, Marco Aurélio S |
collection | PubMed |
description | The aim of this study was to evaluate the effect of overload-induced hypertrophy on extensor digitorum longus (EDL) and soleus muscles of streptozotocin-induced diabetic rats. The overload-induced hypertrophy and absolute tetanic and twitch forces increases in EDL and soleus muscles were not different between diabetic and control rats. Phospho-Akt and rpS6 contents were increased in EDL muscle after 7 days of overload and returned to the pre-overload values after 30 days. In the soleus muscle, the contents of total and phospho-Akt and total rpS6 were increased in both groups after 7 days. The contents of total Akt in controls and total rpS6 and phospho-Akt in the diabetic rats remained increased after 30 days. mRNA expression after 7 days of overload in the EDL muscle of control and diabetic animals showed an increase in MGF and follistatin and a decrease in myostatin and Axin2. The expression of FAK was increased and of MuRF-1 and atrogin-1 decreased only in the control group, whereas Ankrd2 expression was enhanced only in diabetic rats. In the soleus muscle caused similar changes in both groups: increase in FAK and MGF and decrease in Wnt7a, MuRF-1, atrogin-1, and myostatin. Differences between groups were observed only in the increased expression of follistatin in diabetic animals and decreased Ankrd2 expression in the control group. So, insulin deficiency does not impair the overload-induced hypertrophic response in soleus and EDL muscles. However, different mechanisms seem to be involved in the comparable hypertrophic responses of skeletal muscle in control and diabetic animals. |
format | Online Article Text |
id | pubmed-4552534 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2015 |
publisher | John Wiley & Sons, Ltd |
record_format | MEDLINE/PubMed |
spelling | pubmed-45525342015-09-02 Overload-induced skeletal muscle hypertrophy is not impaired in STZ-diabetic rats Fortes, Marco Aurélio S Pinheiro, Carlos Hermano J Guimarães-Ferreira, Lucas Vitzel, Kaio F Vasconcelos, Diogo A A Curi, Rui Physiol Rep Original Research The aim of this study was to evaluate the effect of overload-induced hypertrophy on extensor digitorum longus (EDL) and soleus muscles of streptozotocin-induced diabetic rats. The overload-induced hypertrophy and absolute tetanic and twitch forces increases in EDL and soleus muscles were not different between diabetic and control rats. Phospho-Akt and rpS6 contents were increased in EDL muscle after 7 days of overload and returned to the pre-overload values after 30 days. In the soleus muscle, the contents of total and phospho-Akt and total rpS6 were increased in both groups after 7 days. The contents of total Akt in controls and total rpS6 and phospho-Akt in the diabetic rats remained increased after 30 days. mRNA expression after 7 days of overload in the EDL muscle of control and diabetic animals showed an increase in MGF and follistatin and a decrease in myostatin and Axin2. The expression of FAK was increased and of MuRF-1 and atrogin-1 decreased only in the control group, whereas Ankrd2 expression was enhanced only in diabetic rats. In the soleus muscle caused similar changes in both groups: increase in FAK and MGF and decrease in Wnt7a, MuRF-1, atrogin-1, and myostatin. Differences between groups were observed only in the increased expression of follistatin in diabetic animals and decreased Ankrd2 expression in the control group. So, insulin deficiency does not impair the overload-induced hypertrophic response in soleus and EDL muscles. However, different mechanisms seem to be involved in the comparable hypertrophic responses of skeletal muscle in control and diabetic animals. John Wiley & Sons, Ltd 2015-07-21 /pmc/articles/PMC4552534/ /pubmed/26197932 http://dx.doi.org/10.14814/phy2.12457 Text en © 2015 The Authors. Physiological Reports published by Wiley Periodicals, Inc. on behalf of the American Physiological Society and The Physiological Society. http://creativecommons.org/licenses/by/4.0/ This is an open access article under the terms of the Creative Commons Attribution License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Original Research Fortes, Marco Aurélio S Pinheiro, Carlos Hermano J Guimarães-Ferreira, Lucas Vitzel, Kaio F Vasconcelos, Diogo A A Curi, Rui Overload-induced skeletal muscle hypertrophy is not impaired in STZ-diabetic rats |
title | Overload-induced skeletal muscle hypertrophy is not impaired in STZ-diabetic rats |
title_full | Overload-induced skeletal muscle hypertrophy is not impaired in STZ-diabetic rats |
title_fullStr | Overload-induced skeletal muscle hypertrophy is not impaired in STZ-diabetic rats |
title_full_unstemmed | Overload-induced skeletal muscle hypertrophy is not impaired in STZ-diabetic rats |
title_short | Overload-induced skeletal muscle hypertrophy is not impaired in STZ-diabetic rats |
title_sort | overload-induced skeletal muscle hypertrophy is not impaired in stz-diabetic rats |
topic | Original Research |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4552534/ https://www.ncbi.nlm.nih.gov/pubmed/26197932 http://dx.doi.org/10.14814/phy2.12457 |
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