MOTS-c injections made muscle cells more responsive to insulin by activating AMPK and increasing GLUT4, which helps move glucose into cells.

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Evidence from Studies

Supporting (1)

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The mitochondrial-derived peptide MOTS-c promotes metabolic homeostasis and reduces obesity and insulin resistance

Randomized Controlled Trial

Animal

2015 Mar 3

The study shows that a tiny molecule from mitochondria (MOTS-c) helps mouse muscles use sugar better by turning on a key energy sensor (AMPK), which usually makes more sugar transporters (GLUT4) — so the claim fits what the study found.

Contradicting (0)

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No contradicting evidence found

Source Study

The mitochondrial-derived peptide MOTS-c promotes metabolic homeostasis and reduces obesity and insulin resistance

Score: 13

DOI: 10.1016/j.cmet.2015.02.009

Similar Assertions

MOTS-c made muscle cells produce more GLUT4 (a sugar transporter) and turned on AMPK (an energy sensor), two key players in how muscles use sugar.

86%

Obese mice treated with MOTS-c had lower levels of ANGPTL4 in their muscles, which may help prevent fat buildup.

75%

Mice given MOTS-c had more ANGPTL4 protein in their muscles and less fatty acids, which may help prevent muscle damage from fat buildup.

71%

As mice get older, their bodies make less of a peptide called MOTS-c, especially in muscles and blood—and when they fast, levels drop too, hinting that this peptide responds to energy needs.

71%

MOTS-c reduces visceral and hepatic fat and improves insulin sensitivity even on a high-fat diet by activating AMPK, the cellular energy sensor, which enhances glucose uptake, insulin signaling, and fuel efficiency.

71%