Cholic acid and deoxycholic acid induce skeletal muscle atrophy through a mechanism dependent on TGR5 receptor.
Animals
Cells, Cultured
Cholic Acid
/ pharmacology
Deoxycholic Acid
/ pharmacology
Male
Mice
Mice, Inbred C57BL
Muscle Fibers, Skeletal
/ drug effects
Muscle Proteins
/ metabolism
Muscle, Skeletal
/ drug effects
Muscular Atrophy
/ chemically induced
Myosin Heavy Chains
/ drug effects
Oxidative Stress
/ drug effects
Receptors, G-Protein-Coupled
/ metabolism
Tripartite Motif Proteins
/ metabolism
Ubiquitin-Protein Ligases
/ metabolism
ROS
TGR5 receptor
autophagy
bile acids
muscle atrophy
muscle wasting
ubiquitin-proteasome system
Journal
Journal of cellular physiology
ISSN: 1097-4652
Titre abrégé: J Cell Physiol
Pays: United States
ID NLM: 0050222
Informations de publication
Date de publication:
01 2021
01 2021
Historique:
received:
04
02
2020
revised:
04
05
2020
accepted:
21
05
2020
pubmed:
9
6
2020
medline:
28
8
2021
entrez:
8
6
2020
Statut:
ppublish
Résumé
Skeletal muscle atrophy is characterized by the degradation of myofibrillar proteins, such as myosin heavy chain or troponin. An increase in the expression of two muscle-specific E3 ligases, atrogin-1 and MuRF-1, and oxidative stress are involved in muscle atrophy. Patients with chronic liver diseases (CLD) develop muscle wasting. Several bile acids increase in plasma during cholestatic CLD, among them, cholic acid (CA) and deoxycholic acid (DCA). The receptor for bile acids, TGR5, is expressed in healthy skeletal muscles. TGR5 is involved in the regulation of muscle differentiation and metabolic changes. In this paper, we evaluated the participation of DCA and CA in the generation of an atrophic condition in myotubes and isolated fibers from the muscle extracted from wild-type (WT) and TGR5-deficient (TGR5
Substances chimiques
Gpbar1 protein, mouse
0
Muscle Proteins
0
Receptors, G-Protein-Coupled
0
Tripartite Motif Proteins
0
Deoxycholic Acid
005990WHZZ
Ubiquitin-Protein Ligases
EC 2.3.2.27
Myosin Heavy Chains
EC 3.6.4.1
Cholic Acid
G1JO7801AE
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
260-272Informations de copyright
© 2020 Wiley Periodicals LLC.
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