MOTS-c helped maintain higher activity levels of key muscle signaling proteins (AKT, FOXO1, FOXO3a) in immobilized mice, which are important for muscle health.
Scientific Claim
In male C57BL/6J mice with 8 days of hindlimb cast immobilization, MOTS-c administration (15 mg/kg/day) was associated with higher phosphorylation levels of AKT (Ser473), FOXO1 (Ser256), and FOXO3a (Ser253) in skeletal muscle compared to immobilized control mice.
Original Statement
“MOTS-c administration restored the decrease in phosphorylation of AKT at Ser 473 (P < 0.01, Fig. 3B), FOXO1 at Ser 256 (P < 0.05, Fig. 3C), and FOXO3a at Ser 253 (P < 0.01; Fig. 3E) that was observed in the cast immobilization control group.”
Evidence Quality Assessment
Claim Status
appropriately stated
Study Design Support
Design supports claim
Appropriate Language Strength
association
Can only show association/correlation
Assessment Explanation
The study is an animal cohort with no blinding confirmation, so causal language is inappropriate. The claim uses 'associated with' which correctly reflects the associative evidence.
Evidence from Studies
Supporting (1)
Mitochondrial-derived microprotein MOTS-c attenuates immobilization-induced skeletal muscle atrophy by suppressing lipid infiltration.