When cells made more MOTS-c, they stopped using oxygen as much and started using sugar instead—even though their mitochondria were still intact.
Scientific Claim
In HEK293 cells, MOTS-c overexpression or treatment reduced mitochondrial oxygen consumption and suppressed the TCA cycle, consistent with a Crabtree effect driven by increased glucose uptake.
Original Statement
“MOTS-c-ST cells and HEK293 cells treated with MOTS-c showed the characteristic increased glucose uptake coupled with reduced basal oxygen consumption rate (OCR)... Reduced oxidative capacity was associated with tricarboxylic acid (TCA) cycle dysregulation...”
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 consistent metabolic shift in cell lines under controlled conditions. The language appropriately reflects association within the experimental context.
More Accurate Statement
“In HEK293 cells, MOTS-c overexpression or treatment was associated with reduced mitochondrial oxygen consumption and suppression of the TCA cycle, consistent with a Crabtree effect driven by increased glucose uptake.”
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 the body use energy better and fight obesity, but it doesn’t say anything about slowing down energy production in these specific cells or making them use more sugar like the claim says.