Switching Off One Protein Made Human Cells Burn More Fat in the Lab

Researchers at the Weizmann Institute of Science say a single protein acts as a switch for how cells handle energy. According to ScienceDaily, turning it off made human cells grown in a laboratory burn more fuel, including fats and carbohydrates, and interfered with the process by which immature cells become fat cells.

The protein is called MTCH2 and is nicknamed Mitch. The work is early-stage: it rests on lab-grown cells and on earlier experiments in mice, not on studies of people with obesity. Still, it points toward a different way of thinking about weight loss, one that focuses on how cells use energy rather than on appetite.

What the researchers found

ScienceDaily reported that the team, working with human cells, used genetic engineering to remove MTCH2. The cells began consuming more fuel, and removing the protein could disrupt the development of fat cells from immature precursor cells.

The work was led by a team under Professor Atan Gross, with doctoral student Sabita Chourasia leading the human-cell experiments. The findings were published in The EMBO Journal in January 2025, and ScienceDaily said additional research published later that year provided further evidence that the protein matters for regulating body fat and metabolism.

What earlier mouse experiments showed

The human-cell results build on earlier work by Gross and his colleagues. In those experiments, the team reduced the activity of MTCH2 in the muscles of mice. The genetically modified animals had higher metabolic activity and resisted obesity caused by their diet.

Their muscles also developed more fibers that are good at using oxygen, which helped endurance. According to the report, the mice did better in exercise and stress tests, showed improvements in heart function and had favorable changes in body composition.

How a protein tied to mitochondria could explain it

To understand why one protein would have such wide effects, the researchers looked at mitochondria, the structures inside cells that convert energy from food into a usable form called ATP. Muscles use ATP to contract, and cells rely on it to grow and repair themselves.

Mitochondria are not fixed in shape. They can merge into connected networks or split into smaller units, and that changes how efficiently a cell produces and uses energy. Gross’s team had previously established that Mitch plays a major role in mitochondrial fusion, the merging process.

Without the protein, the mitochondrial network becomes fragmented. The cells can still generate energy, but changes in energy efficiency and demand can push them to consume more fuel. That offers a possible explanation for the unusual metabolism seen in the mice, whose cells appeared to run in a more energy-intensive state rather than conserving energy.

Why scientists want options beyond appetite-based drugs

ScienceDaily noted that medications such as semaglutide and tirzepatide have transformed obesity treatment over the past decade, largely by influencing appetite and the body’s responses to food. But losing weight does not always mean losing only fat. Weight loss can also include a drop in lean body mass, which covers muscle and other tissues.

A 2026 analysis of 20 clinical trials involving 15,782 participants found that lean mass made up approximately 25% to 39% of the weight lost with several widely used weight-loss medications. The researchers behind that analysis found comparable proportional losses with lifestyle interventions, and adding resistance training helped preserve more lean tissue.

Muscle matters because it supports strength, mobility and metabolic health, which is why scientists are exploring ways to reduce body fat while protecting it.

What this means for people trying to lose weight

For now, nothing changes for patients. The Mitch findings come from lab-grown human cells and from mice, and no treatment based on them has been described. ScienceDaily said only that manipulating the protein could eventually offer a way to influence both fat burning and fat accumulation, and that the results raise hopes for a new approach to weight-loss treatment.

The practical significance is conceptual. If a protein that controls how efficiently mitochondria work can be targeted safely, it could one day complement approaches that work on appetite. Whether that can be done in people, and whether it would produce the same benefits seen in the mice, has not been shown.

The mouse experiments also involved reducing the protein in muscle tissue, so how the effects would carry over to people remains an open question. As with any early laboratory finding, the results would need to be repeated and tested in far more complex systems before anyone could judge their value as a therapy.

Around Prague, based on reporting by ScienceDaily