دورية أكاديمية
Hypertrophy Stimulation at the Onset of Type I Diabetes Maintains the Soleus but Not the EDL Muscle Mass in Wistar Rats.
العنوان: | Hypertrophy Stimulation at the Onset of Type I Diabetes Maintains the Soleus but Not the EDL Muscle Mass in Wistar Rats. |
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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. |
References: | Diabetologia. 2015 Aug;58(8):1693-8. (PMID: 26003326) J Appl Physiol (1985). 2005 Feb;98(2):557-64. (PMID: 15465886) Am J Physiol Endocrinol Metab. 2012 May 1;302(10 ):E1210-20. (PMID: 22354783) Am J Pathol. 2011 Mar;178(3):1287-97. (PMID: 21356379) J Physiol. 2011 Apr 1;589(Pt 7):1831-46. (PMID: 21300751) J Appl Physiol (1985). 2010 Jan;108(1):7-13. (PMID: 19779156) Metabolism. 1989 Apr;38(4):348-52. (PMID: 2524636) Cell Death Differ. 2010 Aug;17(8):1254-65. (PMID: 20139895) Nat Commun. 2013;4:2354. (PMID: 23965929) Front Physiol. 2013 Dec 20;4:379. (PMID: 24391596) Am J Physiol Cell Physiol. 2006 Jul;291(1):C185-8. (PMID: 16436469) J Biol Chem. 1995 May 19;270(20):12109-16. (PMID: 7744859) Horm Metab Res. 1983 Jul;15(7):353-4. (PMID: 6350143) PLoS One. 2013 Aug 14;8(8):e71944. (PMID: 23967267) Pediatr Diabetes. 2011 Jun;12(4 Pt 1):345-64. (PMID: 20860561) J Physiol. 2006 Jul 1;574(Pt 1):291-305. (PMID: 16627569) Physiology (Bethesda). 2008 Jun;23:160-70. (PMID: 18556469) PLoS One. 2010 Jul 16;5(7):e11624. (PMID: 20661274) Skelet Muscle. 2011 Jan 24;1(1):4. (PMID: 21798082) Methods. 2001 Dec;25(4):402-8. (PMID: 11846609) Redox Biol. 2015 Aug;5:267-74. (PMID: 26073261) Clin Nutr. 2004 Dec;23(6):1413-7. (PMID: 15556264) Anat Rec. 1997 Feb;247(2):179-88. (PMID: 9025997) Development. 2016 Sep 1;143(17 ):3128-42. (PMID: 27578179) Anat Rec. 1991 Mar;229(3):298-304. (PMID: 2024774) Cell Res. 2011 Nov;21(11):1591-604. (PMID: 21502976) J Physiol. 2011 Oct 1;589(Pt 19):4759-76. (PMID: 21807613) Mol Cell. 2008 Apr 25;30(2):214-26. (PMID: 18439900) Mol Cell. 2004 May 7;14 (3):395-403. (PMID: 15125842) Anal Biochem. 2016 Jul 1;504:38-40. (PMID: 27060530) Biochem Biophys Res Commun. 2010 May 28;396(2):238-45. (PMID: 20399744) Physiol Rep. 2015 Jul;3(7):null. (PMID: 26197932) Am J Physiol Regul Integr Comp Physiol. 2010 Dec;299(6):R1666-75. (PMID: 20926758) Acta Physiol (Oxf). 2006 Jul;187(3):407-18. (PMID: 16776666) FEBS J. 2013 Sep;280(17):4294-314. (PMID: 23517348) J Appl Physiol (1985). 1999 Sep;87(3):1075-82. (PMID: 10484579) J Physiol. 2008 Mar 15;586(6):1731-41. (PMID: 18202101) Scand J Med Sci Sports. 2012 Feb;22(1):24-33. (PMID: 20673252) Cell Tissue Res. 1977 Jul 11;181(2):255-66. (PMID: 141981) N Engl J Med. 2004 Jun 24;350(26):2682-8. (PMID: 15215484) Am J Physiol. 1992 Jan;262(1 Pt 1):E1-5. (PMID: 1733239) Skelet Muscle. 2015 Apr 28;5:14. (PMID: 25949788) J Appl Physiol (1985). 1992 Dec;73(6):2538-43. (PMID: 1490967) Cell Biol Int. 2013 Jan;37(1):29-35. (PMID: 23319319) Cell Mol Life Sci. 2014 Nov;71(22):4361-71. (PMID: 25080109) J Physiol. 2008 Jan 1;586(1):283-91. (PMID: 17974583) Nature. 2005 Feb 3;433(7025):477-80. (PMID: 15690031) J Appl Physiol Respir Environ Exerc Physiol. 1979 Apr;46(4):835-42. (PMID: 457564) Muscle Biol. 1972;1:89-118. (PMID: 4578602) Am J Physiol Endocrinol Metab. 2009 Jul;297(1):E157-64. (PMID: 19435857) Diabetes. 1996 Apr;45(4):440-5. (PMID: 8603765) Exp Physiol. 2008 Nov;93(11):1190-8. (PMID: 18567600) Proc Natl Acad Sci U S A. 1997 Nov 11;94(23):12457-61. (PMID: 9356471) Am J Physiol Cell Physiol. 2015 Dec 1;309(11):C759-66. (PMID: 26423578) Cardiovasc Res. 1999 Sep;43(4):1018-28. (PMID: 10615429) Anal Biochem. 2010 Jun 15;401(2):318-20. (PMID: 20206115) Am J Physiol Cell Physiol. 2005 Oct;289(4):C853-9. (PMID: 15888552) Skelet Muscle. 2011 Feb 01;1(1):6. (PMID: 21798084) Am J Physiol. 1996 Aug;271(2 Pt 1):E340-7. (PMID: 8770029) J Physiol. 1969 Feb;200(3):667-75. (PMID: 5765854) Front Physiol. 2015 Nov 18;6:338. (PMID: 26635624) Diabetologia. 1997 Sep;40(9):1062-9. (PMID: 9300243) Med Sci Sports Exerc. 2006 Nov;38(11):1950-7. (PMID: 17095929) Microsc Microanal. 2012 Feb;18(1):22-34. (PMID: 22221857) Curr Opin Clin Nutr Metab Care. 2012 May;15(3):240-5. (PMID: 22466926) J Clin Invest. 1996 Oct 15;98(8):1703-8. (PMID: 8878419) PLoS One. 2013 Apr 19;8(4):e62190. (PMID: 23620811) Nature. 1997 May 1;387(6628):83-90. (PMID: 9139826) Biochem Biophys Res Commun. 2009 Oct 9;388(1):112-6. (PMID: 19646957) Methods Mol Biol. 2012;798:213-29. (PMID: 22130839) Nat Cell Biol. 2002 Sep;4(9):648-57. (PMID: 12172553) Proteomics Clin Appl. 2016 Jan;10(1):25-38. (PMID: 26140508) Physiol Rep. 2016 Sep;4(18):null. (PMID: 27650250) J Appl Physiol (1985). 2011 Sep;111(3):844-52. (PMID: 21737823) J Biol Chem. 2002 Jul 5;277(27):23977-80. (PMID: 11997383) Diabetes Care. 2004 Oct;27(10):2382-5. (PMID: 15451904) Front Physiol. 2014 Feb 21;5:69. (PMID: 24600408) Am J Physiol. 1999 Jul;277(1 Pt 1):C152-62. (PMID: 10409118) Am J Physiol Endocrinol Metab. 2014 Aug 15;307(4):E365-73. (PMID: 24961241) Diabetes. 2016 Oct;65(10 ):3053-61. (PMID: 27335233) Nat Cell Biol. 2001 Nov;3(11):1014-9. (PMID: 11715023) Diabetes. 1983 Nov;32(11):1035-9. (PMID: 6642086) FASEB J. 2009 Jul;23(7):2264-73. (PMID: 19237506) J Appl Physiol (1985). 2014 Jun 15;116(12):1582-92. (PMID: 24790014) Q J Exp Physiol. 1989 Jan;74(1):65-74. (PMID: 2524084) Cell Rep. 2016 May 10;15(6):1277-90. (PMID: 27134174) FEBS Lett. 2001 Sep 14;505(2):259-63. (PMID: 11566187) Eur J Appl Physiol. 2009 Jun;106(3):389-98. (PMID: 19294408) Matrix. 1989 Aug;9(4):336-42. (PMID: 2677627) |
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 |
تدمد: | 1664-042X |
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DOI: | 10.3389/fphys.2017.00830 |