As people grow older, many notice that their waistlines expand even when their overall weight changes very little. This increase in abdominal fat is more than a cosmetic concern—it has been consistently linked to a higher risk of type 2 diabetes, cardiovascular disease, fatty liver disease, and other chronic health conditions. Although scientists have long recognized this pattern, the biological mechanisms behind it have remained unclear.
Researchers at City of Hope in California have now identified a mechanism that may help explain why abdominal fat increases with age. In a study published in Science, they describe an age-related stem cell population that appears to promote the formation of new fat cells in the abdomen. The findings suggest that aging does not simply enlarge existing fat cells but may also stimulate the continuous production of new ones.
How Aging Changes Abdominal Fat
Working with collaborators at the University of California, Los Angeles (UCLA), the researchers investigated white adipose tissue, the body’s primary fat-storage tissue. White fat stores excess energy and tends to accumulate around the abdomen as people age. Although existing fat cells are known to enlarge over time, the researchers proposed that increased production of new fat cells might also contribute to age-related weight redistribution.
To explore this possibility, they studied adipocyte progenitor cells (APCs), a type of adult stem cell capable of developing into mature fat cells. In experiments involving mice, APCs collected from older animals were transplanted into younger mice. These older stem cells generated substantially more new fat cells than APCs taken from younger mice.
When the researchers performed the opposite experiment by transplanting APCs from young mice into older animals, the younger cells produced relatively few new fat cells. According to the authors, these findings suggest that aging fundamentally alters the stem cells themselves rather than the surrounding tissue environment alone.
An Aging-Specific Stem Cell Population
Using single-cell RNA sequencing—a technique that measures gene activity in individual cells—the researchers examined how APCs changed throughout aging. In young mice, these precursor cells remained relatively inactive. By middle age, however, they became much more active and began producing large numbers of new fat cells, particularly within abdominal fat tissue.
The researchers identified a previously unrecognized population of cells that emerged as the animals aged. They named these cells committed preadipocytes, age-specific (CP-As). According to the study, these aging-associated precursor cells appeared primarily during middle age and demonstrated an especially strong ability to generate new fat cells. Their appearance coincided with the period when abdominal fat increased most rapidly.
The team also investigated the biological signals responsible for this transition. They identified the leukemia inhibitory factor receptor (LIFR) signaling pathway as an important regulator of CP-A development. In older mice, LIFR signaling appeared essential for these age-specific precursor cells to multiply and mature into fat cells, whereas younger animals relied far less on this pathway.
Evidence That Similar Cells Exist in Humans
To determine whether these findings might also apply to humans, the researchers analyzed abdominal fat samples collected from people of different ages. Using the same single-cell sequencing techniques, they identified cell populations that closely resembled the CP-As observed in mice. These cells were more abundant in tissue obtained from middle-aged individuals than in samples from younger donors.
When studied in laboratory experiments, the human CP-A-like cells also showed a greater ability to develop into new fat cells. Although the researchers emphasize that additional clinical studies are needed, these findings suggest that a similar biological process may contribute to age-related abdominal fat accumulation in humans.
The study adds to growing evidence that changes within stem cells themselves—not lifestyle factors alone—may play an important role in the metabolic changes associated with aging.
What the Findings Could Mean for Future Treatments
The researchers propose that targeting the formation or activity of these aging-specific precursor cells could eventually become a new strategy for preventing or treating abdominal obesity. Rather than focusing exclusively on reducing the size of existing fat cells through diet and exercise, future therapies might aim to limit the production of new fat cells as people grow older.
Because the current study was conducted primarily in mice, much more research will be needed before these findings can be translated into clinical practice. Future investigations are expected to examine how hormones, nutrition, and physical activity influence CP-A cells, as well as whether blocking LIFR signaling can safely reduce abdominal fat accumulation without interfering with the pathway’s other biological functions.
For now, experts emphasize that established lifestyle measures—including regular physical activity, a balanced diet, adequate sleep, and maintaining a healthy weight—remain the most effective approaches for limiting excess visceral fat. Nevertheless, a better understanding of the stem cell biology underlying age-related fat accumulation may eventually complement these strategies with more targeted medical treatments.
The findings also highlight an unusual aspect of aging biology. While many adult stem cells gradually lose their regenerative capacity over time, fat progenitor cells appear to become more active with age. According to the researchers, this distinctive pattern may help explain why abdominal obesity becomes increasingly common later in life and reinforces the view that body fat functions as a dynamic, hormonally active tissue rather than simply serving as passive energy storage.
The authors note that additional studies involving more diverse human populations—including people with obesity, diabetes, and other metabolic disorders—will be necessary. If future research confirms that the CP-A pathway plays a central role in age-related abdominal fat gain, it could become an important target for reducing the health risks associated with expanding waistlines in older adults.
