دورية أكاديمية
أعرض في EDS

Hypertrophy Stimulation at the Onset of Type I Diabetes Maintains the Soleus but Not the EDL Muscle Mass in Wistar Rats.

التفاصيل البيبلوغرافية
العنوان: Hypertrophy Stimulation at the Onset of Type I Diabetes Maintains the Soleus but Not the EDL Muscle Mass in Wistar Rats.
المؤلفون: Fortes MAS; Department of Physiology and Biophysics, Institute of Biomedical Sciences, University of São Paulo, São Paulo, Brazil., Scervino MVM; Department of Physiology and Biophysics, Institute of Biomedical Sciences, University of São Paulo, São Paulo, Brazil., Marzuca-Nassr GN; Department of Physiology and Biophysics, Institute of Biomedical Sciences, University of São Paulo, São Paulo, Brazil.; Department of Internal Medicine, Faculty of Medicine, Universidad de La Frontera, Temuco, Chile., Vitzel KF; School of Health Sciences, College of Health, Massey University, Albany, New Zealand., da Justa Pinheiro CH; Department of Physiology and Biophysics, Institute of Biomedical Sciences, University of São Paulo, São Paulo, Brazil., Curi R; Department of Physiology and Biophysics, Institute of Biomedical Sciences, University of São Paulo, São Paulo, Brazil.; Interdisciplinary Post-Graduate Program in Health Sciences, Cruzeiro do Sul University, São Paulo, Brazil.
المصدر: Frontiers in physiology [Front Physiol] 2017 Oct 26; Vol. 8, pp. 830. Date of Electronic Publication: 2017 Oct 26 (Print Publication: 2017).
نوع المنشور: Journal Article
اللغة: English
بيانات الدورية: Publisher: Frontiers Research Foundation Country of Publication: Switzerland NLM ID: 101549006 Publication Model: eCollection Cited Medium: Print ISSN: 1664-042X (Print) Linking ISSN: 1664042X NLM ISO Abbreviation: Front Physiol Subsets: PubMed not MEDLINE
أسماء مطبوعة: Original Publication: Lausanne : Frontiers Research Foundation
مستخلص: Diabetes mellitus induces a reduction in skeletal muscle mass and strength. Strength training is prescribed as part of treatment since it improves glycemic control and promotes increase of skeletal muscle mass. The mechanisms involved in overload-induced muscle hypertrophy elicited at the establishment of the type I diabetic state was investigated in Wistar rats. The purpose was to examine whether the overload-induced hypertrophy can counteract the hypotrophy associated to the diabetic state. The experiments were performed in oxidative (soleus) or glycolytic (EDL) muscles. PI3K/Akt/mTOR protein synthesis pathway was evaluated 7 days after overload-induced hypertrophy of soleus and of EDL muscles. The mRNA expression of genes associated with different signaling pathways that control muscle hypertrophy was also evaluated: mechanotransduction (FAK), Wnt/β-catenin, myostatin, and follistatin. The soleus and EDL muscles when submitted to overload had similar hypertrophic responses in control and diabetic animals. The increase of absolute and specific twitch and tetanic forces had the same magnitude as muscle hypertrophic response. Hypertrophy of the EDL muscle from diabetic animals mostly involved mechanical loading-stimulated PI3K/Akt/mTOR pathway besides the reduced activation of AMP-activated protein kinase (AMPK) and decrease of myostatin expression. Hypertrophy was more pronounced in the soleus muscle of diabetic animals due to a more potent activation of rpS6 and increased mRNA expression of insulin-like growth factor-1 (IGF-1), mechano-growth factor (MGF) and follistatin, and decrease of myostatin, MuRF-1 and atrogin-1 contents. The signaling changes enabled the soleus muscle mass and force of the diabetic rats to reach the values of the control group.
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فهرسة مساهمة: Keywords: electrostimulation; hyperglycemia; muscle mass regulation; muscle strength; protein synthesis; skeletal muscle
تواريخ الأحداث: Date Created: 20171111 Latest Revision: 20200930
رمز التحديث: 20231215
مُعرف محوري في PubMed: PMC5662641
DOI: 10.3389/fphys.2017.00830
PMID: 29123487
قاعدة البيانات: MEDLINE
الوصف
تدمد:1664-042X
DOI:10.3389/fphys.2017.00830