Researchers at the Weizmann Institute of Science have identified a protein that influences how cells manage fat and energy. Disabling the protein, known as MTCH2 or Mitch, increased fat consumption and reduced the formation of new fat cells in human cell experiments. The work builds on earlier findings in mice.
Scientists led by Prof. Atan Gross and doctoral student Sabita Chourasia removed the Mitch protein from human cells using genetic techniques. This caused mitochondria to break apart, making energy production less efficient and forcing cells to burn more fats, carbohydrates, and amino acids for fuel.
The study, published in the EMBO Journal in 2025, also showed that progenitor cells lacking Mitch struggled to develop into mature fat-storing cells. The researchers noted reduced gene expression and energy shortages that hindered fat synthesis.
Earlier mouse experiments had already demonstrated that animals without Mitch gained less weight, built more endurance-related muscle fibers, and resisted obesity. The human cell results suggest Mitch regulates whether fat is stored or used as energy.
The research involved collaborators from the University of Pennsylvania and the University of Texas at San Antonio. It points to a possible pathway for future obesity studies, though no treatment has been developed yet.
