MOTS-c helps slow down a key cellular growth pathway in pancreatic cells.
Scientific Claim
MOTS-c treatment in pancreatic islet cells is associated with reduced mTORC1 signaling pathway activity.
Original Statement
“MOTS-c overexpression in Min6 cells increased both nuclear and mitochondrial MOTS-c under control conditions. However, under H2O2-treated conditions, nuclear MOTS-c increased to a greater extent than mitochondrial MOTS-c, suggesting a mitochondrial-to-nuclear translocation of MOTS-c (Fig. 5g). Simultaneously, augmentation of nuclear MOTS-c inhibited mTORC1 activity, determined by reduced phosphorylation of 4EBP-1, P70S6K1 and mTOR (2448) (Fig. 5g).”
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 used 'inhibited' which implies causation, but the design lacks randomization/blinding confirmation. Corrected to 'associated with' to reflect observational association.
Evidence from Studies
Supporting (1)
Mitochondrial-encoded peptide MOTS-c prevents pancreatic islet cell senescence to delay diabetes