Researchers have identified the MTCH2 protein as a critical control switch for fat metabolism in human cells for the first time.
A team from Israel's Weizmann Institute of Science led the study. They investigated the protein, known informally as 'Mitch,' after previous research showed that blocking it in mice protected against obesity and improved endurance.
In the new work, scientists deleted the Mitch-producing gene in human cells. They observed a sharp increase in cellular respiration-the process cells use to produce energy from nutrients.
Fat cells without MTCH2 (left) have fewer fat drops (green).
The analysis revealed Mitch's core function: it inhibits the fusion of mitochondria, the cell's energy engines. Without it, cells become highly inefficient at processing energy, forcing them to burn carbohydrates, fats, and amino acids more aggressively.
Crucially, cells missing Mitch specifically began breaking down fat from their own membranes for fuel. The absence also disrupted the process of new fat cell formation.
The absence of MTCH2 (right) interferes with mitochondria fusion.
Scientists caution this creates a hypermetabolic, energy-starved state that could stress tissues. However, they call Mitch a 'crucial regulator' and a promising target for future obesity treatment research, which seeks alternatives to drugs like Ozempic that can cause muscle and bone loss.