A protein called Mitch may be one of the body’s hidden metabolic control points. Researchers found that removing it from human cells increases the use of fats and carbohydrates for energy while making it harder for new fat cells to develop—an advance that could eventually inform obesity treatments designed to avoid muscle loss. The new findings extend earlier Mitch research from mice into human cellular models.
The protein’s formal name is MTCH2, and the work comes from a team led by Prof. Atan Gross at Israel’s Weizmann Institute of Science, with doctoral researcher Sabita Chourasia leading the latest study. The researchers genetically silenced Mitch in human cells, then tracked metabolic changes over time and analyzed more than 100 compounds involved in cellular metabolism. Their findings were published in The EMBO Journal. The Weizmann Institute’s account of the research says the altered cells increased respiration and consumed more fats, carbohydrates, and amino acids.
The mechanism involves mitochondria, the structures that generate usable energy inside cells. Mitch helps regulate mitochondrial fusion, allowing these structures to join into larger, efficient networks. When Mitch is absent, that network breaks apart into separate mitochondria that produce energy less efficiently. The cells appear to compensate by consuming fuel at a faster rate, drawing particularly heavily on fat—including fatty material from their own cell membranes.
The same energy shortage also seems to interfere with the creation of fat cells. Human progenitor cells lacking Mitch did not readily develop into mature fat cells, in part because they had less capacity to build the membranes and other cellular materials required for growth and differentiation. The result was a two-sided effect in the laboratory: existing cells burned more fuel, while the cellular pathway that creates additional fat stores was suppressed.
Those results build on an earlier experiment in which Gross’s team reduced Mitch activity in the muscles of mice. The animals showed greater endurance, more muscle fibers, and resistance to obesity even when exposed to a high-fat diet. Their muscle mitochondria became larger and more metabolically active, helping explain why the animals both used more energy and performed better in physical tests. Earlier research from the institute described the mouse findings and connected Mitch to mitochondrial behavior.
That history makes Mitch an intriguing target at a time when weight-loss therapies are often discussed alongside reductions in muscle mass. But the new work remains a cell study, not a human treatment or clinical trial. Removing Mitch caused mitochondria to operate less efficiently and left cells in a sustained energy-deprived state, effects that could create serious safety questions in a whole organism. Any future therapy would need to control where, when, and how strongly Mitch is blocked before researchers can determine whether the promising metabolic effects translate beyond the laboratory.
