Scientists from the Weizmann Institute in Israel have identified a protein called MTCH2, whose deactivation enables cells to burn fat more efficiently without affecting muscle mass.
GLP-1-based weight loss medications, such as Ozempic, have helped numerous people shed pounds in recent years, but they come with a significant drawback: some patients lose not only fat but also muscle mass and bone density. This has driven researchers to continue exploring alternative approaches to combating obesity that avoid such risks.
Back in 2016, investigators discovered that when the production of the MTCH2 protein—informally nicknamed Mitch in the lab—was disabled in mice, the animals did not gain weight even under unfavorable conditions and showed greater endurance. Now, scientists have tested whether a similar mechanism operates in human cells by deactivating the gene responsible for producing this protein in a human cell culture.
Biologist Sabita Chourasia reported that the team tracked changes in over a hundred substances involved in metabolism over the course of several hours. They found that after MTCH2 was eliminated, cells began producing energy more actively using oxygen—a phenomenon they attribute to the heightened endurance observed in mice during earlier experiments.
The study also clarified the protein’s function: MTCH2 influences mitochondria, the cellular structures that generate energy. Normally, mitochondria merge with one another to boost efficiency, but MTCH2 inhibits this process.
When the protein is absent, cells start consuming energy much faster and constantly experience an energy shortfall, leading them to rapidly deplete stores of carbohydrates, fats, and amino acids. This reduces the body’s tendency to accumulate fat deposits. The researchers also noted that these cells particularly rely on fat as an energy source—even breaking down fats that make up cell membranes.
Biologist Atan Gross pointed out that after MTCH2 was removed, the amount of fat in membranes dropped noticeably, while the quantity of substances used for energy production increased. According to him, this indicates that the cell is essentially breaking down its own fat reserves to meet energy needs.
Additionally, the researchers found that the absence of MTCH2 prevents the formation of new fat cells. Building fat tissue requires considerable energy, and cells without this protein are constantly in a state of energy deficit. At the same time, the activity of genes and substances needed to transform ordinary cells into fat cells is reduced, causing the body to generate fewer fat cells and store less fat.
Despite these promising findings, the scientists caution that it is still a long way from developing a viable treatment based on this discovery—experiments have so far only been conducted on cell cultures and, previously, on mice. Furthermore, a persistent energy deficit could place additional strain on tissues and organs, potentially leading to damage. Therefore, future drugs would need to enhance fat burning without imposing such stress on the body.
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