PMID-33554779 – MOTS-c Reduces Myostatin and Muscle Atrophy Signaling
Kumagai H et al. "MOTS-c reduces myostatin and muscle atrophy signaling," American Journal of Physiology – Endocrinology and Metabolism, 2021;320(4):E680-E690. doi:10.1152/ajpendo.00275.2020
Quick Reference
| Property | Value |
|---|---|
| PMID | 33554779 |
| DOI | 10.1152/ajpendo.00275.2020 |
| Year | 2021 |
| Journal | American Journal of Physiology – Endocrinology and Metabolism |
| Study Type | Animal in vivo |
| Evidence Level | V |
| Sample | High-fat diet mouse model + C2C12 myotubes |
| Peptide(s) Studied | MOTS-C |
Key Findings
- MOTS-c reduces high-fat-diet-induced muscle atrophy signaling
- Inhibits myostatin expression through the CK2-PTEN-mTORC2-AKT-FOXO1 pathway
- Decreased muscle loss and atrophy markers in HFD-fed mice
- Prevents palmitic acid-induced atrophy in C2C12 myotubes in vitro
Study Design
Combined in vivo (HFD mice treated with MOTS-c) and in vitro (C2C12 myotube) experiments. Outcomes: myostatin expression, muscle mass, atrophy signaling markers, pathway analysis.
Limitations
- Mouse obesity/atrophy model; human sarcopenia differs
- Pathway analysis in cell lines may not reflect in vivo muscle tissue
- Single dietary stressor model (HFD)
Clinical Relevance
Directly relevant for sarcopenia and obesity-related muscle loss — a large clinical population. The myostatin inhibition pathway provides mechanistic rationale for MOTS-c in body composition protocols. Supports the combination of MOTS-c with exercise and metabolic interventions.
Related
#research #animal-in-vivo #evidence-level-V