MOTS-c helped restore normal activity levels of key muscle proteins (AKT and FOXOs) that are disrupted during immobilization.
Scientific Claim
In male C57BL/6J mice subjected to 8 days of hindlimb immobilization, daily MOTS-c administration (15 mg/kg/day) was associated with normalized phosphorylation levels of AKT (Ser473), FOXO1 (Ser256), and FOXO3a (Ser253) compared to untreated controls.
Original Statement
“MOTS-c administration restored the decrease in phosphorylation of AKT at Ser 473 (P < 0.01), FOXO1 at Ser 256 (P < 0.05), and FOXO3a at Ser 253 (P < 0.01) 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 design supports association claims. The claim uses 'was associated with' and specifies the molecular targets without causal language.
Evidence from Studies
Supporting (1)
Mitochondrial-derived microprotein MOTS-c attenuates immobilization-induced skeletal muscle atrophy by suppressing lipid infiltration.