Exercise training attenuates skeletal muscle fat infiltration and improves insulin pathway of patients with immune-mediated necrotizing myopathies and dermatomyositis

Carregando...
Imagem de Miniatura
Citações na Scopus
0
Tipo de produção
article
Data de publicação
2023
Título da Revista
ISSN da Revista
Título do Volume
Editora
TURKISH LEAGUE AGAINST RHEUMATISM
Citação
ARCHIVES OF RHEUMATOLOGY, v.38, n.2, p.189-199, 2023
Projetos de Pesquisa
Unidades Organizacionais
Fascículo
Resumo
Objectives: This study aims to evaluate the effects of exercise training on intramuscular lipid content and genes related to insulin pathway in patients with systemic autoimmune myopathies (SAMs). Patients and methods: Between January 2016 and May 2019, a total of seven patients with dermatomyositis (DM; 3 males, 4 females; mean age: 49.8 & PLUSMN;2.3 years; range, 43 to 54 years), six with immune mediated necrotizing myopathy (IMNM; 3 males, 3 females; mean age: 58.5 & PLUSMN;10.6 years; range, 46 to 74 years), and 10 control individuals (CTRL group; 4 males, 6 females; mean age: 48.7 & PLUSMN;3.9 years; range, 41 to 56 years) were included. The muscle biopsy before and after the intervention was performed to evaluate the intramuscular lipid content. Patients underwent a combined exercise training program for 12 weeks. Skeletal muscle gene expression was analyzed and the DM versus CTRL group, DM pre-and post-, and IMNM pre-and post-intervention were compared. Results: The DM group had a higher intramuscular lipid content in type II muscle fibers compared to the CTRL group. After the intervention, there was a reduction of lipid content in type I and II fibers in DM and IMNM group. The CTRL group showed a significantly higher expression of genes related to insulin and lipid oxidation pathways (AMPK$2, AS160, INSR, PGC1-a, PI3K, and RAB14) compared to the DM group. After exercise training, there was an increase gene expression related to insulin pathway and lipid oxidation in DM group (AMPK$2, AS160, INSR, PGC1-a, PI3K, and RAB14) and in IMNM group (AKT2, AMPK$2, RAB10, RAB14, and PGC1-a). Conclusion: Exercise training attenuated the amount of fat in type I and II muscle fibers in patients with DM and IMNM and increased gene expression related to insulin pathways and lipid oxidation in DM and IMNM. These results suggest that exercise training can improve the quality and metabolic functions of skeletal muscle in these diseases.
Palavras-chave
Exercise training, fat infiltration, insulin resistance, myopathies, myositis
Referências
  1. Akazawa N, 2018, PLOS ONE, V13, DOI 10.1371/journal.pone.0201789
  2. Akazawa N, 2017, GERIATR GERONTOL INT, V17, P1683, DOI 10.1111/ggi.12869
  3. Benatti FB, 2018, FRONT IMMUNOL, V9, DOI 10.3389/fimmu.2018.00906
  4. Brons C, 2017, EUR J ENDOCRINOL, V176, pR67, DOI 10.1530/EJE-16-0488
  5. Coley W, 2012, ARTHRITIS RES THER, V14, DOI 10.1186/ar3791
  6. Correia JC, 2015, TRENDS ENDOCRIN MET, V26, P305, DOI 10.1016/j.tem.2015.03.010
  7. Curiel RV, 2009, ANN NY ACAD SCI, V1154, P101, DOI 10.1111/j.1749-6632.2009.04386.x
  8. Dalakas MC, 2011, NEUROPATH APPL NEURO, V37, P226, DOI 10.1111/j.1365-2990.2010.01153.x
  9. Dastmalchi M, 2007, ARTHRIT RHEUM-ARTHR, V57, P1303, DOI 10.1002/art.22996
  10. Day J, 2017, SEMIN ARTHRITIS RHEU, V46, P642, DOI 10.1016/j.semarthrit.2016.11.001
  11. de Moraes MT, 2013, ARTHRIT CARE RES, V65, P793, DOI 10.1002/acr.21879
  12. de Oliveira DS, 2019, CLIN RHEUMATOL, V38, P3435, DOI 10.1007/s10067-019-04738-4
  13. de Oliveira DS, 2019, AUTOIMMUN REV, V18, P315, DOI 10.1016/j.autrev.2018.11.003
  14. de Souza JM, 2019, CLIN EXP RHEUMATOL, V37, P235
  15. Dobin A, 2013, BIOINFORMATICS, V29, P15, DOI 10.1093/bioinformatics/bts635
  16. Glass CK, 2012, CELL METAB, V15, P635, DOI 10.1016/j.cmet.2012.04.001
  17. Goodpaster BH, 2008, J APPL PHYSIOL, V105, P1498, DOI 10.1152/japplphysiol.90425.2008
  18. Hoogendijk Jessica E, 2004, Neuromuscul Disord, V14, P337, DOI 10.1016/j.nmd.2004.02.006
  19. Isenberg DA, 2004, RHEUMATOLOGY, V43, P49, DOI 10.1093/rheumatology/keg427
  20. Khoja SS, 2018, ARTHRIT CARE RES, V70, P333, DOI 10.1002/acr.23278
  21. Kjobsted R, 2017, DIABETES, V66, P598, DOI 10.2337/db16-0530
  22. Liao Y, 2014, BIOINFORMATICS, V30, P923, DOI 10.1093/bioinformatics/btt656
  23. Linklater H, 2013, CLIN EXP RHEUMATOL, V31, P767
  24. Londhe P, 2015, BONE, V80, P131, DOI 10.1016/j.bone.2015.03.015
  25. Louche K, 2013, J CLIN ENDOCR METAB, V98, P4863, DOI 10.1210/jc.2013-2058
  26. Lundberg IE, 2002, RHEUM DIS CLIN N AM, V28, P799, DOI 10.1016/S0889-857X(02)00025-X
  27. Lundberg IE, 2017, ANN RHEUM DIS, V76, P1955, DOI 10.1136/annrheumdis-2017-211468
  28. Meyer A, 2017, ACTA NEUROPATHOL, V134, P655, DOI 10.1007/s00401-017-1731-9
  29. Oliveira Diego Sales de, 2018, MedicalExpress (São Paulo, online), V5, pmo18003, DOI 10.5935/medicalexpress.2018.mo.003
  30. Perandini LA, 2018, FEBS J, V285, P1973, DOI 10.1111/febs.14417
  31. Petersen KF, 2006, AM J MED, V119, p10S, DOI 10.1016/j.amjmed.2006.01.009
  32. Poulsen KB, 2017, CLIN RHEUMATOL, V36, P2289, DOI 10.1007/s10067-017-3706-6
  33. Puigserver P, 2005, INT J OBESITY, V29, pS5, DOI 10.1038/sj.ijo.0802905
  34. Reimers Carl D., 1997, Current Opinion in Rheumatology, V9, P475, DOI 10.1097/00002281-199711000-00002
  35. Richter EA, 2013, PHYSIOL REV, V93, P993, DOI 10.1152/physrev.00038.2012
  36. Rivas DA, 2016, AM J PHYSIOL-REG I, V310, pR561, DOI 10.1152/ajpregu.00198.2015
  37. Samuel VT, 2016, J CLIN INVEST, V126, P12, DOI 10.1172/JCI77812
  38. Samuel VT, 2012, CELL, V148, P852, DOI 10.1016/j.cell.2012.02.017
  39. Scarpulla RC, 2011, BBA-MOL CELL RES, V1813, P1269, DOI 10.1016/j.bbamcr.2010.09.019
  40. Wiesinger GF, 2000, ARCH PHYS MED REHAB, V81, P1, DOI 10.1016/S0003-9993(00)90212-0
  41. Wiggs MP, 2015, FRONT PHYSIOL, V6, DOI 10.3389/fphys.2015.00063
  42. Yao L, 2012, AM J ROENTGENOL, V198, pW475, DOI 10.2214/AJR.11.7113