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.

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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 mice use sugar better by activating a cellular energy sensor (AMPK), which naturally helps muscles take in more sugar—so it supports the idea that it works through these known pathways.

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

86%

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.

74%

When mice were given a daily shot of a peptide called MOTS-c, their bodies became better at using sugar for energy and responding to insulin, especially in their muscles.

74%

MOTS-c activates AMP-activated protein kinase (AMPK), leading to improved glucose uptake, insulin sensitivity, and metabolic efficiency independent of growth hormone signaling.

72%

Mice given MOTS-c burned more sugar for energy and produced more body heat—even though they didn’t move around more than the control mice.

71%