MOTS-c injections made muscle cells more responsive to insulin by activating AMPK and increasing GLUT4, which helps move glucose into cells.
Scientific Claim
In skeletal muscle of mice fed a high-fat diet, MOTS-c treatment was associated with increased phosphorylation of AMPK at Thr172 and higher GLUT4 protein levels.
Original Statement
“MOTS-c promoted AMPK activation and GLUT4 expression in the skeletal muscles of HFD-fed mice (Figure 6G).”
Evidence Quality Assessment
Claim Status
overstated
Study Design Support
Design supports claim
Appropriate Language Strength
association
Can only show association/correlation
Assessment Explanation
The study uses causal language ('promoted') but the design is limited to mice and cell lines, which cannot establish causation in humans. The claim should reflect association only.
Evidence from Studies
Supporting (1)
The mitochondrial-derived peptide MOTS-c promotes metabolic homeostasis and reduces obesity and insulin resistance
The study shows that a tiny molecule from mitochondria (MOTS-c) helps mouse muscles use sugar better by turning on a key energy sensor (AMPK), which usually makes more sugar transporters (GLUT4) — so the claim fits what the study found.