From left: Prof. Myoung-Gon Ko of Ulsan National Institute of Science and Technology (UNIST), researchers Seong-Jun Byun, Chan-Hyung Lee, and Gyu-Min Jang. Provided by UNIST.
The principle by which fat cells in the body enhance the heat-producing capacity of mitochondria, the “stoves inside cells,” has been identified. The finding is expected to provide a stepping stone for developing obesity treatments that make fat cells consume more energy.
Ulsan National Institute of Science and Technology (UNIST) announced on the 3rd that a research team led by Prof. Myoung-Gon Ko in the Department of Biological Sciences has discovered that the protein “TET” is a gene-regulating protein that links mitochondrial degradation in fat cells with heat production in adipose tissue
In adipose tissue in the body, there is white fat that stores excess fat and brown fat that burns energy to generate heat. When exposed to cold, some of the white fat that had been storing excess fat is converted into “beige fat,” which burns fat and produces heat like brown fat.
The research team uncovered the mechanism by which beige fat regulates genes that enhance the heat-producing capacity of mitochondria.
When exposed to cold, the level of TET protein in fat cells decreases. As TET levels fall, the amount of “Parkin,” a protein that selectively eliminates mitochondria, also decreases. Parkin attaches a degradation tag to mitochondria so that the cellular cleaning system can recognize them as targets for removal. When Parkin levels drop, the rate of mitochondrial degradation slows, and more mitochondria used for heat production remain inside the cell
Under normal conditions, TET directly binds to the Parkin gene, removes methylation (the attachment of a methyl group to DNA), and helps the Parkin gene be properly expressed (protein production). When cold exposure reduces TET, methylation accumulates again on Parkin DNA, blocking the production of Parkin protein.
The research team kept a mouse model, genetically engineered so that TET protein is not produced in fat cells, at 4 ℃ for one week. As a result, they confirmed that Parkin protein levels in the mice decreased, while mitochondrial DNA—a marker used to estimate mitochondrial abundance—and proteins involved in cellular respiration increased.
In cell-level experiments, when normal Parkin protein was introduced under conditions where TET was inhibited, the increased mitochondrial content and oxygen consumption returned to their original levels. This outcome shows that TET regulates Parkin, and Parkin in turn governs mitochondrial degradation and energy expenditure.
Prof. Ko said, “It has been known that exposure to cold increases mitochondria in fat cells and activates heat production, but the upstream regulatory factor that controls these changes had not been clearly identified. Our study has now clarified this,” adding, “These findings can be applied to research on treatments for metabolic diseases that induce fat cells to consume more energy.” The results were published online on July 1 in the international journal Metabolism.
<Reference>doi.org/10.1016/j.metabol.2026.156685
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