New medicines for weight loss can help people drop pounds, but they often also shrink muscle. Researchers have now found a natural way that might do the opposite – burn more fat while protecting muscle.
Meet MTCH2, the “Mitch” Protein
Scientists at the Weizmann Institute of Science studied a protein called MTCH2, which they nicknamed “Mitch.” In lab tests, turning off Mitch made human cells use more energy from fats and sugars. At the same time, the cells made fewer new fat cells.
What Happened in Mice?
Earlier work with mice gave a big clue. When the researchers blocked Mitch in mouse muscles, the animals stayed thin, ran longer, and built stronger muscle fibers. The mice also showed better heart function.
These surprising results made the team wonder how one protein could affect both weight and stamina.
Power Plants Inside Cells: Mitochondria
Inside every cell are tiny structures called mitochondria – the cell’s power plants. Mitochondria can join together into long networks that work efficiently, or stay separate as small units that work less efficiently. When they are less efficient, cells have to burn more fuel – fats, carbs, and proteins – to keep going.
Gross’s team discovered that Mitch helps mitochondria stay fused. Without Mitch, the networks break apart, making energy production harder.
Removing Mitch from Human Cells
Graduate student Sabita Chourasia used gene‑editing tools to delete the Mitch gene from human cells. The result was dramatic.
- Mitochondria split into many tiny pieces.
- Energy production became less efficient, putting cells in a constant “low‑energy” state.
- To survive, the cells started burning more fuel.
“We saw a big rise in cellular respiration – the process that turns food into energy – after removing Mitch,” Chourasia said. “That explains why the mice with less Mitch could run longer.”
Fat Becomes the Main Fuel
Because the altered cells needed extra energy, they ate more fat, carbs, and amino acids. However, they relied most heavily on fat. The scientists also noticed that the amount of fat stored in cell membranes dropped, while the amount of fat used for energy rose.
In short, Mitch acts like a switch that decides whether fat is saved or burned.
Blocking New Fat Cell Formation
Obese women often have higher levels of Mitch. The researchers wondered if the protein also helps create new fat cells. Fat cells grow from precursor cells called progenitors. When Mitch was removed from these progenitors, they struggled to turn into mature fat cells.
Without Mitch, the cells couldn’t build the membranes they need to store fat, and the genes that drive this process were turned down. The result: fewer new fat cells and less overall fat storage.
Why This Matters for Obesity Research
The study was done only in cells, so it is not yet a therapy. Still, it shows a powerful pathway that can both increase fat burning and stop new fat cells from forming. Targeting Mitch could someday give doctors a way to treat obesity without losing muscle.
The research was a collaboration between the Weizmann Institute of Science, the University of Pennsylvania, and the University of Texas at San Antonio.