Scientists discover a protein switch that burns fat and blocks new fat cells
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- Weizmann Institute scientists identified protein MTCH2 (nicknamed "Mitch") as a regulator of cellular energy management and fat storage, publishing the findings in The EMBO Journal
- Prof. Atan Gross and doctoral student Sabita Chourasia found that deleting Mitch from human cells increased fat and carbohydrate burning while simultaneously reducing formation of new fat cells
- The discovery builds on earlier mouse studies in which animals lacking Mitch in muscle tissue became leaner, developed more oxygen-consuming muscle fibers, showed greater endurance, and had improved heart function
- Mitch controls mitochondrial fusion — without it, mitochondrial networks fragment into smaller, less efficient units, forcing cells into a chronic energy shortage that drives higher fuel consumption from fats, carbs, and amino acids
- Women with obesity tend to have elevated Mitch levels, and removing the protein from progenitor cells blocked their transformation into mature fat-storing cells by suppressing differentiation genes and limiting membrane synthesis
- The work involved collaborators from the University of Pennsylvania and the University of Texas at San Antonio, and could eventually address the muscle-loss side effect of modern weight-loss drugs
Why it matters: Modern weight-loss drugs reduce lean muscle alongside fat. The Weizmann team showed disabling MTCH2 in human cells forces them to burn more fat while simultaneously blocking new fat-cell formation — a dual-action pathway that, if it translates from cell studies to humans, could preserve muscle while shedding weight, though clinical use remains years away.
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