Browse evidence-based analysis of health-related claims and assertions
If the drug doesn’t shrink your belly fat by 8%, it won’t make your fat healthier-looking on scans — you have to respond to the drug for this benefit.
Doctors use CT scans to measure how dense fat is — denser fat means the fat cells are smaller and healthier, even if you can’t see them directly.
The study mostly included men who are white — so we don’t know if the drug works the same way in women or people of other races.
If the drug doesn’t shrink your belly fat by at least 8%, it won’t make your fat look healthier on scans — you have to respond to the drug for this benefit.
The drug makes the fat around the organs healthier-looking on scans more than the fat under the skin — it works better on belly fat than on thigh or arm fat.
Before treatment, the fat under the skin looked just as healthy on scans in both the drug and placebo groups — so any changes later were caused by the drug.
Before starting the drug, the fat quality in the group that got the drug was just like the group that got the placebo — so any differences later were due to the treatment.
Only HIV patients whose belly fat shrinks by at least 8% after taking this drug also get healthier-looking fat on scans — others don’t benefit in this way.
The fat under the skin gets denser and healthier-looking on scans even when the amount of that fat doesn’t change much — the drug is improving its quality directly.
Even when scientists account for how much belly fat was lost, the fat that’s left still gets denser and healthier-looking on scans — meaning the drug is doing something beyond just shrinking fat.
The same drug that reduces belly fat in HIV patients also makes the fat under the skin denser and healthier-looking on scans, even when the amount of fat doesn’t change much.
For HIV patients with belly fat who respond to this drug, the fat becomes denser and healthier-looking on scans after 6 months of treatment, even if the amount of fat doesn’t change much.
MOTS-c didn’t make mice move more, so its effects on weight and metabolism aren’t just because they were exercising more.
MOTS-c made mouse cells break down more fat for fuel, as shown by higher levels of fat-burning byproducts and lower levels of stored fats.
When scientists changed two specific letters in the MOTS-c peptide, it stopped working—proving those spots are essential for its sugar-burning effect.
A few days of MOTS-c shots in mice lowered levels of two proteins linked to inflammation, hinting it might help calm down the body’s immune response.
The MOTS-c peptide is almost the same in humans, mice, rats, and other animals—especially in four key spots—meaning evolution kept it because it’s important for how the body uses energy.
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.
When cells made more MOTS-c, they stopped using oxygen as much and started using sugar instead—even though their mitochondria were still intact.
Old mice that got MOTS-c injections responded to insulin just as well as young mice, meaning the peptide might fix the insulin resistance that comes with aging.
When scientists removed the mitochondria’s DNA from human cells, the MOTS-c peptide disappeared—proving it comes from the mitochondria, not the cell’s main DNA.
Scientists found MOTS-c in the blood of humans and mice, and when they fasted, the levels dropped—hinting it might be a hormone that tells the body how to use energy.
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.
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.