魏茨曼科学研究所的研究人员发现了一种名为MTCH2的蛋白质，该蛋白质在脂肪代谢和能量消耗中起关键作用1。通过关闭这种蛋白质，研究团队发现人类细胞会消耗更多脂肪、碳水化合物和氨基酸1。在动物实验中，敲除小鼠肌肉组织中的MTCH2导致能量消耗增加、耐力提高、抗肥胖性增强1。
在脂肪细胞形成方面的发现更为显著1。正常前驱脂肪细胞中80%-90%会在6天内分化成成熟脂肪细胞，而缺乏MTCH2的细胞中仅有5%-10%完成这一过程1。进一步研究表明，MTCH2通过调控CPT1酶活性来影响脂肪酸进入线粒体的过程1。在高脂肪饮食试验中，脂肪组织中缺乏MTCH2的小鼠体重增长较少，但进食量保持相同，瘦体质量也未出现变化1。
原始研究由Atan Gross教授和Sabita Chourasia博士领导，发表于2025年1月3日的《The EMBO Journal》1。后续研究则在2025年10月3日发表于《Nature Communications》上，进一步深化了对该蛋白质作用机制的理解1。
Researchers at the Weizmann Institute of Science have identified a protein called MTCH2, nicknamed "Mitch," that plays a critical role in regulating fat metabolism and energy expenditure.1 Disabling this protein causes cells to burn significantly more fat and carbohydrates while preventing the formation of new fat cells, according to findings published in The EMBO Journal on January 3, 2025, and led by Professor Atan Gross and Dr. Sabita Chourasia.1
In laboratory studies, blocking MTCH2 function produced dramatic metabolic effects.1 When the protein was removed from human cells, they consumed substantially greater quantities of fat, carbohydrates, and amino acids.1 In mouse muscle tissue, MTCH2 elimination increased energy expenditure and endurance while enhancing resistance to obesity.1 Most strikingly, while 80–90% of normal precursor fat cells differentiate into mature fat cells within six days, only 5–10% of cells lacking MTCH2 completed this transformation.1
Subsequent research published in Nature Communications on October 3, 2025, revealed the molecular mechanism underlying these effects: MTCH2 regulates the activity of the CPT1 enzyme, which controls how fatty acids enter mitochondria.1 In mice genetically lacking MTCH2 in fat tissue, body weight gain was substantially reduced when fed a high-fat diet despite consuming the same amount of food, while lean muscle mass remained unchanged.1
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