Anyone who has grown older knows the quiet shift: rooms that once felt comfortable now seem chilled, and the body is slower to answer the cold. City of Hope researchers, reporting in Nature, have traced part of that change to thermogenic fat, the tissue that burns energy to make warmth, and found that its responsiveness dims with age in mice. The work points beneath the familiar experience of feeling the weather more, toward a body whose internal heat-making has grown slow to switch on, and it opens a door, still far from any clinic, toward restoring that lost warmth and perhaps the metabolic
Fading Thermogenic Fat Activity May Explain Why Aging Bodies Feel the Cold More
Still able to turn up the heat, but slower to do it
Mark
So what did the researchers actually find?
Mimi
That a kind of fat built to make heat gets slower to respond as animals age. In older mice it still worked, but it took longer to turn up when the cold hit.
Mark
And that's tied to the cells inside that fat?
Mimi
Yes. Some cells have a lot of UCP1, the heat-generating protein, and some have less. Nerve and immune signals shift the balance between them depending on how much warmth is needed.
Luke
Worth being clear that most of this was done in mice. Human fat samples showed a similar mix of cells, but that's not the same as showing humans lose heat the same way.
Mark
So the title's claim about aging bodies is a hypothesis?
Mimi
The source says it "may explain" it. That's careful wording, and it should stay that way.
Mark
What about the drug?
Mimi
Mifepristone blocked one part of the pathway and older mice made more heat and burned more energy.
Luke
But it affects many parts of the body, and the researchers say it isn't a treatment. It's a tool showing the slowdown can be reversed, not a remedy.
Mark
Why does Wang bring up diabetes and obesity?
Mimi
Because thermogenic fat also burns glucose and fat. If its decline contributes to metabolic problems, restoring it could matter well beyond feeling warm.
Luke
And that's a "could eventually." Nothing here shows it yet.
El Pulso
- Older bodies are losing their ability to answer the cold, as heat-producing fat responds more slowly with each passing year.
- Inside thermogenic fat, a mix of highly active and sluggish cells normally shifts heat output on demand, but in older mice that switching has stalled.
- Older mice struggled to hold their body temperature in the cold, revealing how far the slowdown reaches into everyday survival.
- Blocking one pathway with mifepristone brought back some lost heat production, but researchers stress the drug is a probe, not a remedy.
- The path forward runs through safe, precise therapies, and the findings still await proof beyond mice, with human samples showing only a similar cell mix.
Anyone who has grown older knows the quiet shift: rooms that once felt comfortable now seem chilled, and the body is slower to answer the cold. City of Hope researchers, reporting in Nature, have traced part of that change to thermogenic fat, the tissue that burns energy to make warmth, and found that its responsiveness dims with age in mice. The work points beneath the familiar experience of feeling the weather more, toward a body whose internal heat-making has grown slow to switch on, and it opens a door, still far from any clinic, toward restoring that lost warmth and perhaps the metabolic health it touches.
Most people past a certain age have noticed it: the house feels colder than it used to. A new study in Nature, led by researchers at City of Hope, one of the largest cancer research and treatment organizations in the United States, offers a biological reason why.
The focus is thermogenic fat, which differs from the white fat that mostly stores energy. Thermogenic fat burns calories to create heat, and its activity tends to decline with age, which may help explain why older people feel the cold more sharply.
Qiong "Annabel" Wang, an associate professor at City of Hope's Arthur Riggs Diabetes & Metabolism Research Institute and the corresponding author, has shown that signals from nerves and immune cells decide how much heat this tissue produces by adjusting the balance between highly active and less active fat cells. The less active cells can be pushed to raise their output when warmth is needed, then turned back down when it is not.
In older mice, that adjustment became sluggish. The fat could still generate heat, but more slowly, and the animals had trouble keeping their temperature steady in the cold. When the team blocked one part of the pathway behind the slowdown with mifepristone, the older mice produced more heat and burned more energy. The drug acts broadly, so it is not a treatment, but the result suggests the decline may be reversible.
Wang sees implications beyond warmth. Thermogenic fat also burns glucose and fat, and its waning activity may be tied to age-related problems such as obesity and type 2 diabetes. For now, these are mouse findings, though human samples show a similar mix of cells. The open questions are whether more targeted ways to restore this fat can be found and whether they hold up outside the lab.
Ask almost anyone past a certain age and they will tell you the same thing: the house feels colder than it used to. A new study published in Nature, from researchers at City of Hope, one of the largest cancer research and treatment organizations in the United States, offers a biological explanation for why that happens.
The focus is thermogenic fat, a kind of body fat that works differently from the white fat most people think of. White fat mainly stores energy. Thermogenic fat burns calories to make heat and helps keep the body warm. Its activity tends to decline with age, which may be part of why older people are more sensitive to cold.
The corresponding author is Qiong "Annabel" Wang, Ph.D., an associate professor at City of Hope's Arthur Riggs Diabetes & Metabolism Research Institute. Her work shows how signals from nerves and immune cells set how much heat thermogenic fat produces. They do it by changing the balance between highly active and less active fat cells.
That variation among cells was something City of Hope researchers had already found. Some thermogenic fat cells carry high levels of UCP1, a protein that generates heat. Others carry less UCP1 and stay less active. In the new study, the team saw a similar mix in samples of human thermogenic fat, though most of the experiments were done in mice.
The mixture appears to give the body a built-in way to adjust to temperature. When more warmth is needed, signals from the nervous and immune systems push the less-active cells to raise their heat output. When the need passes, the system can turn that activity back down.
In older mice, that adjustment became sluggish. Their thermogenic fat could still ramp up heat production, but it took longer to do so. The animals had more trouble holding their body temperature when exposed to cold.
The researchers then blocked one part of the biological pathway behind the slowdown, using the drug mifepristone. The treated older mice produced more heat and burned more energy, so some of the lost heat production was restored. Mifepristone acts on many parts of the body, so it is not a treatment for age-related cold sensitivity. But the result suggests the decline in thermogenic fat activity could be reversed.
Wang said the possibility matters beyond staying warm. Thermogenic fat also burns glucose and fat, and its activity tends to fall with age. If scientists can find a safe, precise way to restore it, she said, this foundational research could deepen understanding of age-related metabolic problems, including obesity and type 2 diabetes.
For now, the findings are mouse findings, with human samples showing a similar cell mix. What to watch for is whether more targeted ways of restoring thermogenic fat activity can be found, and whether they hold up beyond the lab.
Citas Notables
Thermogenic fat also burns glucose and fat, and its activity tends to decline with age; a safe, precise way to restore it could deepen understanding of age-related metabolic problems.— Qiong "Annabel" Wang, Ph.D., City of Hope
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