Ursodeoxycholic acid induces sarcopenia associated with decreased protein synthesis and autophagic flux.
Autophagic flux
Bile acids
Protein synthesis
Sarcopenia
Ursodeoxycholic acid
Journal
Biological research
ISSN: 0717-6287
Titre abrégé: Biol Res
Pays: England
ID NLM: 9308271
Informations de publication
Date de publication:
27 May 2023
27 May 2023
Historique:
received:
01
02
2023
accepted:
13
04
2023
medline:
29
5
2023
pubmed:
27
5
2023
entrez:
26
5
2023
Statut:
epublish
Résumé
Skeletal muscle generates force and movements and maintains posture. Under pathological conditions, muscle fibers suffer an imbalance in protein synthesis/degradation. This event causes muscle mass loss and decreased strength and muscle function, a syndrome known as sarcopenia. Recently, our laboratory described secondary sarcopenia in a chronic cholestatic liver disease (CCLD) mouse model. Interestingly, the administration of ursodeoxycholic acid (UDCA), a hydrophilic bile acid, is an effective therapy for cholestatic hepatic alterations. However, the effect of UDCA on skeletal muscle mass and functionality has never been evaluated, nor the possible involved mechanisms. We assessed the ability of UDCA to generate sarcopenia in C57BL6 mice and develop a sarcopenic-like phenotype in C UDCA induced sarcopenia in healthy mice, evidenced by decreased strength, muscle mass, and physical function, with a decline in the fiber's diameter and the troponin I protein levels. In the C Our results indicate that UDCA induces sarcopenia in mice and sarcopenic-like features in C
Sections du résumé
BACKGROUND
BACKGROUND
Skeletal muscle generates force and movements and maintains posture. Under pathological conditions, muscle fibers suffer an imbalance in protein synthesis/degradation. This event causes muscle mass loss and decreased strength and muscle function, a syndrome known as sarcopenia. Recently, our laboratory described secondary sarcopenia in a chronic cholestatic liver disease (CCLD) mouse model. Interestingly, the administration of ursodeoxycholic acid (UDCA), a hydrophilic bile acid, is an effective therapy for cholestatic hepatic alterations. However, the effect of UDCA on skeletal muscle mass and functionality has never been evaluated, nor the possible involved mechanisms.
METHODS
METHODS
We assessed the ability of UDCA to generate sarcopenia in C57BL6 mice and develop a sarcopenic-like phenotype in C
RESULTS
RESULTS
UDCA induced sarcopenia in healthy mice, evidenced by decreased strength, muscle mass, and physical function, with a decline in the fiber's diameter and the troponin I protein levels. In the C
CONCLUSIONS
CONCLUSIONS
Our results indicate that UDCA induces sarcopenia in mice and sarcopenic-like features in C
Identifiants
pubmed: 37237400
doi: 10.1186/s40659-023-00431-8
pii: 10.1186/s40659-023-00431-8
pmc: PMC10224307
doi:
Substances chimiques
Ursodeoxycholic Acid
724L30Y2QR
Ribosomal Protein S6 Kinases, 70-kDa
EC 2.7.11.1
Troponin I
0
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
28Subventions
Organisme : Fondo Nacional de Desarrollo Científico y Tecnológico
ID : 1200944
Organisme : Fondo Nacional de Desarrollo Científico y Tecnológico
ID : 1201039
Organisme : Agencia Nacional de Investigación y Desarrollo (ANID) - Millennium Science Initiative Program - ICN09_016 / ICN 2021_045: Millennium Institute on Immunology and Immunotherapy
ID : ICN09_016 / ICN 2021_045
Organisme : Agencia Nacional de Investigación y Desarrollo (ANID) - Millennium Science Initiative Program - ICN09_016 / ICN 2021_045: Millennium Institute on Immunology and Immunotherapy
ID : former P09/016-F
Organisme : Agencia Nacional de Investigación y Desarrollo (ANID) - Millennium Science Initiative Program - ICN09_016 / ICN 2021_045: Millennium Institute on Immunology and Immunotherapy
ID : ICN09_016 / ICN 2021_045
Organisme : Agencia Nacional de Investigación y Desarrollo (ANID) - Millennium Science Initiative Program - ICN09_016 / ICN 2021_045: Millennium Institute on Immunology and Immunotherapy
ID : former P09/016-F
Organisme : Vicerrectoría de Investigación y Doctorado, Universidad Andrés Bello, Proyecto Iniciación a la Investigación
ID : DI-03-21/INI
Organisme : Vicerrectoría de Investigación y Doctorado, Universidad Andrés Bello, Proyecto Iniciación a la Investigación
ID : DI-05-21/INI
Organisme : Beca ANID
ID : 21201447
Organisme : Beca ANID
ID : 21212005
Organisme : Beca ANID
ID : 21212221
Informations de copyright
© 2023. The Author(s).
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