When cells made extra MOTS-c, they had 20 times more AICAR, which turned on AMPK, a key energy regulator.
Scientific Claim
In HEK293 cells stably overexpressing MOTS-c, AICAR levels were 20-fold higher than in control cells, leading to AMPK activation.
Original Statement
“accumulation of endogenous AICAR to levels higher than 20-fold in MOTS-c-ST cells compared to control cells (Figure 3A, E)”
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 ('leading to AMPK activation') but the design is limited to cell lines, which cannot establish causation in humans. The claim should reflect association only.
More Accurate Statement
“In HEK293 cells stably overexpressing MOTS-c, AICAR levels were 20-fold higher than in control cells and associated with AMPK activation.”
Evidence from Studies
Supporting (0)
Contradicting (1)
The mitochondrial-derived peptide MOTS-c promotes metabolic homeostasis and reduces obesity and insulin resistance
The study says MOTS-c helps cells use energy better by turning on AMPK, but it never talks about AICAR or the type of cells mentioned in the claim, so the claim adds details that aren't in the research.