Scientists Just Found a Secret Switch That Turns Off Fat Storage—And Turns On Fat Burning

3 min readObesity impacts 40 percent of adults in the U.S. and is a key driver of disease in the western world.A new study analyzed a protein named MTCH2, or Mitch, and its impact on human cells and found that suppressing the protein’s expression helped burn fat faster while decreasing the accumulation of fat cells.This study comes a decade after the same team analyzed how MTCH2 impacted mice, with similar results.For the past 50 years, a majority of the Western world has been in the grips of an obesity epidemic. The rise of ultra-processed foods as well as the arrival of more sedentary lifestyles, whether working in an office or driving in traffic for hours a day, have created a troubling scenario where an estimated 40 percent of adults in the U.S. struggle with obesity.While diet and exercise remain key to keeping weight gain in check, science has recruited valuable allies in recent years in the fight against this growing epidemic. The most well-known is glucagon-like peptide-1, or GLP-1, a synthetic hormone that sends signals to your brain when you’re full. Inspired by the discovery of Exendin-4, which is a peptide hormone found in the venom of the Gila monster, GLP-1 forms the foundation of medications such as Wegovy and Ozempic. However, this might not be the only tool scientists can use to fix obesity.In a new study published in The European Molecular Biology Organization (EMBO) Journal, a team of scientists led by researchers at the Weizmann Institute of Science in Israel explored the slimming power of a protein called MTCH2, or “Mitch.” Typically, Mitch plays a key role in apoptosis (programmed cell death), mitochondrial dynamics, and metabolism, but for more than a decade, the study’s senior author, Atan Gross, has studied how suppressing the expression of this protein increased the rate at which fats and carbohydrates burn, while inhibiting the creation of new fat cells.“We discovered that deleting Mitch led to a major drop in fats in membranes,” Gross said in a press statement. “At the same time, we saw an increase in fatty substances used to produce energy, and we realized that the fat was being broken down from the membrane to be used as fuel. In other words, we showed that Mitch determines the fate of fat in human cells.”In 2016, Gross and his team published the results of MTCH2 suppression in mice, showing that Mitch is a “pivotal regulator of muscle metabolism and whole-body energy homeostasis” and hinting that further investigation of the protein could aid in the fight against metabolic diseases, such as diabetes, as well as obesity. In the new study, Gross and his team, including lead author Sabita Chourasia, tested how human cells react to similar Mitch suppression and found that, as in mice, energy production in the cells declined, which increased the body’s use of fat deposits.“We saw an increase in cellular respiration, the process in which the cell produces energy from nutrients, such as carbohydrates and fats, using oxygen,” Chourasia said in the press statement. “This explains the increase in muscular endurance in previous experiments using mice.”Additionally, the authors explored the role Mitch plays in storing fat. Knowing that women with obesity have increased levels of Mitch, they hypothesized that the protein must play a role in cell differentiation. They found that Mitch helped progenitor cells (partially differentiated cells at an intermediate stage between stem cells and mature cells) accumulate fat and become mature fat cells. Once Mitch was suppressed, the accumulation of mature fat cells declined. “The process of fat accumulation requires a large amount of available energy, but in cells without Mitch, there is a shortage of energy,” Gross says.In our deep biological past, the MTCH2 protein helped keep early humans alive by providing an energy safety net when times were scarce, but in the face of abundant food supplies in the 21st century, it’s maladapted. If new therapies could one day align Mitch with today’s biological realities, the obesity epidemic could finally come to an end.Darren lives in Portland, has a cat, and writes/edits about sci-fi and how our world works. You can find his previous stuff at Gizmodo and Paste if you look hard enough.