Plate Nº 47 · recorded October 10, 2026
Health & Medicine ResearchReported finding
Mitochondrial switch links body clock, cold, and diet to fat burning
A Danish team has tied fat-cell energy use to one mitochondrial protein whose levels jump 90-fold in the cold. The discovery points to a new way of treating obesity and type 2 diabetes.
By Nathan Brooks3 min read572 words
In brief
- Study published in Science (2026), DOI 10.1126/science.adz4797, by CBMR at the University of Copenhagen
- After 24 hours in the cold, SLC25A34 levels in mouse brown fat rose 90-fold
- Three independent signals converge on the Slc25a34 gene: the clock protein REV-ERBα, cold, and dietary fat via PPARα
- Silencing SLC25A34 reduced fuel burning in brown-fat cells from 3 of 4 human donors
- Across 24 clinical studies, higher SLC25A34 in subcutaneous white fat correlated with leanness and healthier metabolism
Brown fat produces heat by burning fuel. Now researchers have identified one mitochondrial protein — SLC25A34 — that links the body's circadian clock, the surrounding temperature, and meals into a single fat-burning response. Their findings appeared in Science (2026; DOI: 10.1126/science.adz4797).
The work comes from the NNF Center for Basic Metabolic Research (CBMR) at the University of Copenhagen. Corresponding author Zach Gerhart-Hines, an associate professor at CBMR, said: "We usually think of the body clock, the response to temperature and the response to food as separate systems. A mitochondrial transporter that is tuned by the time of day, the temperature and what we eat raises the possibility of therapies that shift when and how the body burns fuel."
What does cold reveal about the protein?
The cold triggered the discovery. Mice housed at room temperature kept almost no SLC25A34 in their brown fat — less than nearly every other organ. After 24 hours in the cold, levels of the protein jumped 90-fold, making brown fat the richest source of SLC25A34 in the body.
What does the cold have to do with the body clock?
The team screened large datasets for proteins in mouse brown fat that respond to both the clock and cold. Only two candidates cleared every test: UCP1, the well-known heat-producing protein, and SLC25A34, a related transporter of unknown function.
Using mice engineered to lack specific regulatory proteins, the researchers found three independent controls on the Slc25a34 gene:
- The clock protein REV-ERBα keeps the gene silent during sleep and releases it before waking.
- Cold removes this brake at any hour, overriding the schedule when extra heat becomes urgent.
- Dietary fat — from the tissue's own stores or from food — turns the gene on through a separate regulator called PPARα.
Why do fasting and insulin boost the same transporter?
That was the puzzle. Fasting signals fat use; insulin signals fat storage. Yet both raise SLC25A34. The resolution is how active brown fat operates: it builds new fat molecules and then burns them on the spot. Each cycle clears fat and sugar from the blood while producing heat. SLC25A34 appears to keep the recycling going by carrying oxaloacetate back into the mitochondria.
Mice lacking SLC25A34 burned less fuel, and their brown fat responded to cold more weakly than normal animals. The team has not yet proven that the transporter directly carries oxuloacetate, and the long-term consequences of losing it remain unknown.
Does the finding hold up in humans?
In the lab, silencing SLC25A34 in human brown-fat cells from donors reduced fuel burning in three of four samples. Across 24 clinical studies, people with more SLC25A34 in subcutaneous white fat tended to be leaner and to have healthier metabolic markers. That link is correlation, not proof of causation.
First author Iuliia Karavaeva of CBMR summed up the wider horizon: "Many of these mitochondrial transporters still have no known function. This one turned out to be needed both for building fat and for burning it. And we are only scratching the surface: SLC25A34 is also highly expressed in the heart and is implicated in brain and liver metabolism, but what it does in those organs remains a mystery."
The group now plans to test whether drugs can dial SLC25A34 up or down, an approach that would diverge from today's obesity and diabetes drugs and instead aim at when and how the body burns fuel.
via Medical Xpress (Source)
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