# Scientists find the aging switch that helps belly fat grow

> Researchers at City of Hope have identified a stem-cell change that may help explain why waistlines often expand in middle age. The study, published in Science, found that aging can activate a newly recognized population of fat-making cells that appears to boost...

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Byline: City of Hope
Published: 2026-07-08T11:41:56+00:00
Categories: Health

![Close-up of hands gripping an overweight belly, depicting body fat focus](https://www.argo.net/wp-content/uploads/2026/06/belly_fat_anatomy.jpg)

Researchers at [City of Hope](https://www.eurekalert.org/news-releases/1081786) have identified a stem-cell change that may help explain why waistlines often expand in middle age. The study, published in **Science**, found that aging can activate a newly recognized population of fat-making cells that appears to boost the production of new belly fat cells.

The finding matters because abdominal fat is strongly tied to metabolic problems that become more common with age. Many people gain fat around the midsection while their overall body weight changes only modestly. The new work points to a cellular process that may help drive that familiar shift.

"People often lose muscle and gain body fat as they age, even when their body weight remains the same," said **Qiong (Annabel) Wang**, Ph.D., a co-corresponding author of the study and an associate professor of molecular and cellular endocrinology at City of Hope's Arthur Riggs Diabetes & Metabolism Research Institute.

## A stem cell shift in middle age

The research focused on **white adipose tissue**, the body's main fat-storage tissue. This tissue holds energy in the form of fat and plays a major role in weight gain. Around the abdomen, it is also closely linked with type 2 diabetes, heart disease and other age-related health risks.

Scientists already knew that existing fat cells can swell as the body stores more energy. The City of Hope team looked at another route to fat growth. They examined whether aging also pushes fat tissue to create entirely new fat cells.

To investigate that question, the researchers studied **adipocyte progenitor cells**. These are stem-like cells inside fat tissue that can mature into adipocytes, the cells that store fat. In young animals, these cells were comparatively quiet. In middle age, they became far more active.

That change gave the team a possible explanation for expanding waistlines during aging. Fat tissue may grow because older progenitor cells start producing new fat cells at a high rate. The effect was especially important in abdominal fat, the form most closely tied to metabolic disease.

## Why older fat tissue makes new fat cells

The team used mouse experiments to separate the age of the cell from the age of the body surrounding it. Researchers transplanted progenitor cells from young and older mice into young mice. Cells from older animals generated many new fat cells after transplantation.

Then the researchers reversed the experiment. When progenitor cells from young mice were transplanted into older mice, they produced far fewer new fat cells. That result suggested that the powerful fat-making behavior was carried by the older cells themselves.

**Adolfo Garcia-Ocana**, Ph.D., chair of the Department of Molecular and Cellular Endocrinology at City of Hope, described the pattern as a reversal of what many people expect from aging stem cells. "Aging unlocks these cells' power to evolve and spread," he said.

This part of the study is important because it narrows the search for a biological driver. The surrounding tissue environment matters in aging, yet these experiments showed that the aged progenitor cells had acquired their own strong tendency to create fat.

The work also helps explain why body composition can shift even when the number on the scale seems stable. A person can lose muscle and gain fat at the same time. That tradeoff can leave body weight looking similar while abdominal fat increases.

## The newly found CP-A cells

To see what was changing inside the cells, the scientists used **single-cell RNA sequencing**. This method reads gene activity cell by cell. It allows researchers to detect hidden cell populations that can be missed when many cells are blended into one average signal.

The analysis revealed a newly identified population called **committed preadipocytes, age-specific**, or CP-As. These cells appeared with aging and showed a strong ability to become fat cells. They emerged from the broader pool of adipocyte progenitor cells as mice reached middle age.

"We discovered aging triggers the arrival of a new type of adult stem cell," Wang said. In the study, these CP-A cells were especially efficient at producing new fat cells. Their appearance gave the researchers a concrete cellular target for age-related fat growth.

The name CP-A reflects what the cells seem prepared to do. They are already committed to the fat-cell pathway and they appear in an age-linked pattern. That makes them a useful clue for understanding why belly fat can increase as animals grow older.

The discovery also changes the way scientists may think about fat tissue during aging. Fat tissue is a living organ with many cell types. Some of those cells can change behavior as the body ages and CP-As appear to be part of that remodeling.

## LIFR emerges as a key signal

After identifying CP-A cells, the researchers looked for signals that might control their behavior. One pathway stood out: **LIFR**, short for leukemia inhibitory factor receptor. Receptors act like molecular antennas on cells. They receive signals that can change what a cell does next.

In this case, LIFR appeared to help CP-A cells multiply and develop into fat cells. The researchers found that older mice relied on this signal for the age-linked burst of fat-cell formation. Younger mice showed a different pattern of fat production.

"Our research indicates that LIFR plays a crucial role in triggering CP-As to create new fat cells," Wang said. That finding makes LIFR an especially interesting target for future research.

A target is useful only after scientists understand where it acts and what might happen if it is blocked. The City of Hope work suggests that LIFR is tied to the specific CP-A program seen in aging fat tissue. That gives researchers a starting point for testing whether the pathway can be adjusted safely.

For now, the evidence comes mainly from preclinical experiments in mice and cellular analyses. That early stage matters. A biological target can look promising in the lab and still require years of testing before it can guide a treatment for people.

## Human cells show a similar pattern

The researchers also examined **human tissue samples** from people of different ages. Using the same single-cell approach, they found cells that resembled the CP-A population seen in mice. These cells were more common in tissue from middle-aged individuals.

That human evidence strengthens the relevance of the mouse findings. It suggests that a similar age-linked fat-making program may exist in people. The study also found that the human CP-A-like cells had a strong capacity to generate new fat cells.

Still, the human portion of the work should be read with care. Cell studies can show a plausible mechanism, while clinical outcomes require additional evidence. Researchers will need to learn how CP-A-like cells behave in living human tissue over time.

The connection to abdominal fat is especially important because belly fat can act as a metabolically active tissue. It can influence inflammation, insulin sensitivity and broader metabolic health. That makes the origin of new fat cells a significant question for aging research.

The study's combination of mouse experiments and human-cell analysis gives scientists a more detailed map of the process. It links aging, a specific progenitor-cell state and a signal pathway that helps drive fat-cell formation.

## A possible target for healthier aging

The discovery offers a possible route toward addressing **age-related belly fat** at its cellular source. If CP-A cells help fuel abdominal fat growth, then future therapies might aim to block their formation, reduce their activity, or interrupt signals that push them toward fat production.

Such ideas remain in the research stage. The study does point to clear next steps. Scientists can track CP-A cells in animal models, study their behavior in human tissue and test whether LIFR-related signals can be altered without disrupting healthy fat function.

Fat tissue has essential jobs. It stores energy, helps regulate hormones and communicates with other organs. Any future therapy would need to target harmful age-linked fat expansion while preserving the useful roles of fat tissue.

For researchers studying **metabolic disorders**, the new work provides a more precise question. Instead of viewing middle-age belly fat only as a broad shift in metabolism, scientists can now examine a defined cell population and a named signaling pathway.

That precision could matter for healthier aging. As Wang noted, understanding how CP-A cells emerge and function could eventually lead to medical strategies that reduce abdominal fat and improve long-term metabolic health. The path from discovery to therapy is still ahead, but the cellular switch is now in clearer view.