Scientists discover a hidden switch that burns fat and blocks new fat cells
Scientists have discovered that switching off a protein called Mitch makes human cells burn more fat and prevents new fat cells from developing. The breakthrough builds on experiments in mice that showed remarkable resistance to obesity and improved muscular endurance, raising hopes for a new approach to weight-loss treatment.
Key points
- Researchers at the Weizmann Institute of Science identified a protein called MTCH2, or Mitch, that influences whether cells burn or store fat.
- Disabling MTCH2 increased fat and carbohydrate consumption in human cells and reduced fat cell formation in mouse precursor cells.
- In mice, removing MTCH2 from fat tissue increased energy expenditure and protected against weight gain on a high-fat diet.
Scientists at the Weizmann Institute of Science have identified a protein called MTCH2, nicknamed Mitch, that plays a key role in controlling metabolism. When researchers disabled this protein in laboratory experiments, cells consumed more fuel, including fats and carbohydrates, and the process through which immature cells develop into fat cells was disrupted.
The findings, published in The EMBO Journal in January 2025, build on earlier experiments in mice where switching off Mitch in muscle tissue increased energy expenditure, improved endurance and protected the animals from diet-related obesity. Additional research published later in 2025 provided further evidence of the protein's importance in regulating body fat and metabolism.
How Mitch affects fat cells
In experiments with mouse precursor fat cells, deleting MTCH2 sharply reduced differentiation: approximately 80% to 90% of normal precursor cells differentiated within six days, compared with only 5% to 10% of cells lacking MTCH2. The altered cells also accumulated substantially fewer lipid droplets.
Professor Atan Gross explained that cells without Mitch face an energy shortage and suppressed expression of genes needed for differentiation, so new fat cell formation is reduced. The fat cell experiments used a mouse-derived cell line, while nutrient consumption analysis was conducted in human cells.
We discovered that deleting Mitch led to a major drop in fats in membranes
— Professor Atan Gross
Follow-up study in fat tissue
Research published on October 3, 2025, in Nature Communications found that MTCH2 helps regulate the movement of fatty acids into mitochondria by interacting with the enzyme CPT1. Removing MTCH2 altered this control system, allowing mitochondria to increase fatty acid utilization and energy expenditure.
When researchers removed MTCH2 specifically from the fat cells of mice, the animals burned more energy without increasing physical activity or changing food intake. On a high-fat diet, these mice gained less weight and body fat than untreated mice, while their lean body mass remained comparable.
