Scientists discover a protein switch that burns fat and blocks new fat cells
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- Weizmann Institute researchers identified MTCH2 ("Mitch"), a protein that regulates mitochondrial fusion and determines whether fat is stored or burned in human cells.
- Human cells without Mitch showed broken-apart mitochondrial networks that created energy inefficiency, forcing cells to consume more fats, carbohydrates, and amino acids as fuel.
- Cells lacking Mitch shifted to burning fat as their primary fuel source, with researchers observing major drops in membrane fats being repurposed for energy production.
- Progenitor cells without Mitch failed to differentiate into mature fat-storing cells because the resulting energy shortage suppressed differentiation genes and blocked the membrane synthesis needed for fat accumulation.
- Earlier mouse studies in Prof. Atan Gross's lab had shown that animals lacking Mitch in muscle tissue became leaner, developed more muscle fibers, and showed better endurance and heart function.
- The study, led by doctoral student Sabita Chourasia and published in The EMBO Journal, involved collaborators from the University of Pennsylvania and the University of Texas at San Antonio.
Why it matters: Modern weight loss drugs often strip muscle along with fat, a drawback the source explicitly identifies as the problem Mitch-targeting therapy could address. By burning existing fat stores while preventing new fat cell formation, the pathway offers a dual-action mechanism — though the work remains in cell studies, years from any clinical trial.
