Advanced search
1 file | 3.92 MB Add to list

Carnosine and skeletal muscle dysfunction in a rodent multiple sclerosis model

Author
Organization
Abstract
Muscle weakness and fatigue are primary manifestations of multiple sclerosis (MS), a chronic disease of the central nervous system. Interventions that enhance muscle function may improve overall physical well-being of MS patients. Recently, we described that levels of carnosine, an endogenous muscle dipeptide involved in contractile function and fatigue-resistance, are reduced in muscle tissue from MS patients and a monophasic rodent MS model (experimental autoimmune encephalomyelitis, EAE). In the present study, we aimed to (1) confrm this fnding in a chronic EAE model, along with the characterization of structural and functional muscle alterations, and (2) investigate the efect of carnosine supplementation to increase/restore muscle carnosine levels and improve muscle function in EAE. We performed muscle immunohistochemistry and ex vivo contractility measurements to examine muscle structure and function at diferent stages of EAE, and following nutritional intervention (oral carnosine: 3, 15 or 30 g/L in drinking water). Immunohistochemistry revealed progressively worsening muscle fber atrophy and a switch towards a fast-twitch muscle phenotype during EAE. Using ex vivo muscle contractility experiments, we observed reductions in muscle strength and contraction speed, but no changes in muscle fatigability of EAE mice. However, carnosine levels were unaltered during all stages of EAE, and even though oral carnosine supplementation dose-dependently increased muscle carnosine levels up to+94% after 56 days EAE, this did not improve muscle function of EAE mice. In conclusion, EAE mice display signifcant, yet time-dependent, muscular alterations, and carnosine intervention does not improve muscle function in EAE.
Keywords
Organic Chemistry, Clinical Biochemistry, Biochemistry, Multiple sclerosis, Experimental autoimmune encephalomyelitis, Carnosine, Histidine-containing dipeptides, Skeletal muscle, BETA-ALANINE SUPPLEMENTATION, EXERCISE, ENCEPHALOMYELITIS, PERFORMANCE, THERAPY, FATIGUE, DISEASE

Downloads

  • (...).pdf
    • full text (Published version)
    • |
    • UGent only
    • |
    • PDF
    • |
    • 3.92 MB

Citation

Please use this url to cite or link to this publication:

MLA
Spaas, Jan, et al. “Carnosine and Skeletal Muscle Dysfunction in a Rodent Multiple Sclerosis Model.” AMINO ACIDS, 2021, doi:10.1007/s00726-021-03086-5.
APA
Spaas, J., Van Noten, P., Keytsman, C., Nieste, I., Blancquaert, L., Derave, W., & Eijnde, B. O. (2021). Carnosine and skeletal muscle dysfunction in a rodent multiple sclerosis model. AMINO ACIDS. https://doi.org/10.1007/s00726-021-03086-5
Chicago author-date
Spaas, Jan, Pieter Van Noten, Charly Keytsman, Ine Nieste, Laura Blancquaert, Wim Derave, and Bert O. Eijnde. 2021. “Carnosine and Skeletal Muscle Dysfunction in a Rodent Multiple Sclerosis Model.” AMINO ACIDS. https://doi.org/10.1007/s00726-021-03086-5.
Chicago author-date (all authors)
Spaas, Jan, Pieter Van Noten, Charly Keytsman, Ine Nieste, Laura Blancquaert, Wim Derave, and Bert O. Eijnde. 2021. “Carnosine and Skeletal Muscle Dysfunction in a Rodent Multiple Sclerosis Model.” AMINO ACIDS. doi:10.1007/s00726-021-03086-5.
Vancouver
1.
Spaas J, Van Noten P, Keytsman C, Nieste I, Blancquaert L, Derave W, et al. Carnosine and skeletal muscle dysfunction in a rodent multiple sclerosis model. AMINO ACIDS. 2021;
IEEE
[1]
J. Spaas et al., “Carnosine and skeletal muscle dysfunction in a rodent multiple sclerosis model,” AMINO ACIDS, 2021.
@article{8723366,
  abstract     = {{Muscle weakness and fatigue are primary manifestations of multiple sclerosis (MS), a chronic disease of the central nervous system. Interventions that enhance muscle function may improve overall physical well-being of MS patients. Recently, we described that levels of carnosine, an endogenous muscle dipeptide involved in contractile function and fatigue-resistance, are reduced in muscle tissue from MS patients and a monophasic rodent MS model (experimental autoimmune encephalomyelitis, EAE). In the present study, we aimed to (1) confrm this fnding in a chronic EAE model, along with the characterization of structural and functional muscle alterations, and (2) investigate the efect of carnosine supplementation to increase/restore muscle carnosine levels and improve muscle function in EAE. We performed muscle immunohistochemistry and ex vivo contractility measurements to examine muscle structure and function at diferent stages of EAE, and following nutritional intervention (oral carnosine: 3, 15 or 30 g/L in drinking water). Immunohistochemistry revealed progressively worsening muscle fber atrophy and a switch towards a fast-twitch muscle phenotype during EAE. Using ex vivo muscle contractility experiments, we observed reductions in muscle strength and contraction speed, but no changes in muscle fatigability of EAE mice. However, carnosine levels were unaltered during all stages of EAE, and even though oral carnosine supplementation dose-dependently increased muscle carnosine levels up to+94% after 56 days EAE, this did not improve muscle function of EAE mice. In conclusion, EAE mice display signifcant, yet time-dependent, muscular alterations, and carnosine intervention does not improve muscle function in EAE.}},
  author       = {{Spaas, Jan and Van Noten, Pieter and Keytsman, Charly and Nieste, Ine and Blancquaert, Laura and Derave, Wim and Eijnde, Bert O.}},
  issn         = {{0939-4451}},
  journal      = {{AMINO ACIDS}},
  keywords     = {{Organic Chemistry,Clinical Biochemistry,Biochemistry,Multiple sclerosis,Experimental autoimmune encephalomyelitis,Carnosine,Histidine-containing dipeptides,Skeletal muscle,BETA-ALANINE SUPPLEMENTATION,EXERCISE,ENCEPHALOMYELITIS,PERFORMANCE,THERAPY,FATIGUE,DISEASE}},
  language     = {{eng}},
  pages        = {{13}},
  title        = {{Carnosine and skeletal muscle dysfunction in a rodent multiple sclerosis model}},
  url          = {{http://dx.doi.org/10.1007/s00726-021-03086-5}},
  year         = {{2021}},
}

Altmetric
View in Altmetric
Web of Science
Times cited: