MOTS-c made muscle cells produce more GLUT4 (a sugar transporter) and turned on AMPK (an energy sensor), two key players in how muscles use sugar.
Scientific Claim
In mice, MOTS-c treatment increased skeletal muscle GLUT4 expression and AMPK phosphorylation, linking its metabolic effects to known regulators of glucose transport and energy balance.
Original Statement
“MOTS-c promoted AMPK activation and GLUT4 expression in the skeletal muscles of HFD-fed mice... MOTS-c treatment led to the phosphorylation of AMPKα (Thr172)...”
Evidence Quality Assessment
Claim Status
overstated
Study Design Support
Design cannot support claim
Appropriate Language Strength
association
Can only show association/correlation
Assessment Explanation
The study uses causal language ('promoted') but the evidence is limited to mouse tissue and cell models. Only an associative interpretation is valid.
More Accurate Statement
“In mice, MOTS-c treatment was associated with increased skeletal muscle GLUT4 expression and AMPK phosphorylation, linking its metabolic effects to known regulators of glucose transport and energy balance.”
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 mice use sugar better by activating a cellular energy sensor (AMPK), which naturally helps muscles take in more sugar—so it supports the idea that it works through these known pathways.