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.
Scientific Claim
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.
Original Statement
“So tesamellin works upstream through growth hormone and IGF signaling and then MOS works inside the cell in the trenches directly at the level of the mitochondrial metabolism. So there's a study in cell metabolism that showed that MOS C reduced visceral fat, reduced liver fat, and improved insulin sensitivity even on a poor diet. But the mechanism was different. Instead of stimulating growth hormone pathways, MOT C activated AMPK, which is the cell's energy sensor. So improving glucose uptake, insulin signaling, and fuel efficiency.”
Context Details
Domain
pharmacology
Population
animal
Subject
MOTS-c
Action
reduces
Target
visceral and hepatic fat and improves insulin sensitivity by activating AMPK
Intervention Details
Evidence from Studies
Supporting (3)
Mitochondrial-derived microprotein MOTS-c attenuates immobilization-induced skeletal muscle atrophy by suppressing lipid infiltration.
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
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.
Targeting colonic macrophages improves glycemic control in high-fat diet-induced obesity
This study found that targeting certain immune cells in the gut can improve blood sugar control in obese mice, which supports the idea that MOTS-c can improve insulin sensitivity by affecting similar pathways.