MOTS-c injections made mice burn more glucose instead of fat, as shown by higher CO2 output relative to oxygen use.
Scientific Claim
In mice fed a high-fat diet, MOTS-c treatment was associated with increased respiratory exchange ratio (RER), indicating higher glucose utilization.
Original Statement
“MOTS-c treated mice also generated significantly more heat that may, in part, account for the increased energy expenditure (Figure 6I). Total activity was comparable between the 2 groups (Figure S6). MOTS-c was also able to prevent HFD-induced obesity and hyperinsulinemia independent of caloric intake in C57BL/6 mice (Figure S7). These studies suggest that MOTS-c prevents HFD-induced obesity by increasing energy expenditure, including heat production, and improving glucose utilization and insulin sensitivity. Reduced fat accumulation may be a result of robust carbohydrate usage that reduces fatty acid synthesis, but the possible involvement of increased fatty acid oxidation, as observed in vitro, would need detailed examination before being ruled out.”
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 ('prevents HFD-induced obesity by increasing energy expenditure') but the design is limited to mice and cell lines, which cannot establish causation in humans. The claim should reflect association only.
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 mice stay healthy on a high-fat diet, but it never measured whether they burned more sugar instead of fat, which is what the claim is about.