MOTS-c, a mitochondrial peptide, reduces visceral and liver fat and improves insulin sensitivity even on a poor diet by activating AMPK, the cell’s energy sensor, which improves glucose uptake and fuel efficiency.

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Evidence from Studies

Supporting (2)

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Mitochondrial-derived microprotein MOTS-c attenuates immobilization-induced skeletal muscle atrophy by suppressing lipid infiltration.

Randomized Controlled Trial

Animal

2024 Mar 1

This study found that MOTS-c helps prevent muscle loss and improves lipid metabolism in mice, which supports the idea that MOTS-c can improve insulin sensitivity.

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

Randomized Controlled Trial

Animal

2015 Mar 3

This study found that a tiny molecule from mitochondria, called MOTS-c, helps mice stay healthy even when eating lots of fat by turning on a cellular energy switch (AMPK) that improves how the body uses sugar and stores less fat.

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Similar Assertions

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

83%

Mice that ate a fatty diet and got daily MOTS-c shots didn’t get as fat as mice that didn’t get the shots—even though they ate the same amount of food.

75%

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.

74%

MOTS-c injections reduced fat buildup in the livers of mice eating a high-fat diet, as seen in tissue samples.

72%

Obese mice given MOTS-c injections for three days had lower blood sugar levels than mice that didn't receive the treatment.

71%