When scientists added MOTS-c to cells in a dish, the cells started using more sugar for energy and turned on a key energy sensor called AMPK—until they added folic acid or blocked AMPK, which stopped the effect.
Scientific Claim
In HEK293 and L6 myotube cells, MOTS-c treatment increased glycolytic flux and AMPK phosphorylation, which was reversed by folic acid supplementation or AMPK inhibition, suggesting a mechanism involving folate cycle suppression and AMPK activation.
Original Statement
“MOTS-c treatment led to the phosphorylation of AMPKα (Thr172)... co-treatment with folic acid fully reversed this effect... knock-down of AMPKα2 alone and AMPKα1/2 showed a 16% and 30% decrease in glucose-stimulated glycolytic rate...”
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 demonstrates a sequence of molecular events in cell lines using controlled interventions. While mechanistic, the findings are confined to in vitro models and cannot be generalized as universal mechanisms.
More Accurate Statement
“In HEK293 and L6 myotube cells, MOTS-c treatment was associated with increased glycolytic flux and AMPK phosphorylation, which was reversed by folic acid supplementation or AMPK inhibition, suggesting a mechanism involving folate cycle suppression and AMPK activation.”
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 mitochondrial protein called MOTS-c helps cells burn sugar better by turning on an energy sensor (AMPK) and slowing down a related chemical process (folate cycle), which matches what the claim says.