Researchers have uncovered a previously unknown biological mechanism that may explain why belly fat tends to increase with age, even in people whose body weight remains relatively stable. The findings, published in Science, identify a new type of stem cell that emerges during aging and appears to drive the formation of new abdominal fat cells.

The study, led by scientists at City of Hope in collaboration with UCLA, suggests that age-related weight gain is not simply caused by existing fat cells becoming larger. Instead, aging activates a specialized population of stem cells that dramatically increases the body's capacity to produce entirely new fat cells.

To investigate this process, researchers focused on white adipose tissue, the body's primary fat storage tissue, and examined adipocyte progenitor cells (APCs)—stem cells that can develop into mature fat cells.

Experiments in mice revealed that APCs taken from older animals generated significantly more new fat cells than those from young mice, regardless of the age of the recipient. This suggests that aging fundamentally changes the stem cells themselves, making them far more efficient at producing fat.

Using single-cell RNA sequencing, the researchers discovered that aging also gives rise to a previously unknown population of stem cells called age-specific committed preadipocytes (CP-As). These cells appear primarily during middle age and possess an exceptional ability to generate new fat cells, particularly in abdominal tissue.

Further analysis identified the leukemia inhibitory factor receptor (LIFR) signaling pathway as a critical regulator of this process. While young mice were able to produce fat without relying on this pathway, older mice depended on LIFR to activate CP-As and stimulate fat formation.

The scientists then examined human fat tissue and identified cells closely resembling CP-As. These cells were found more frequently in samples from middle-aged individuals and also demonstrated a strong ability to produce new fat cells, suggesting that the same biological mechanism may occur in humans.

According to the researchers, the discovery opens new possibilities for treating age-related obesity. Future studies will investigate how CP-As develop, how they contribute to metabolic diseases, and whether therapies that block or eliminate these cells could help prevent abdominal fat accumulation during aging.

Although additional research is needed before clinical applications become available, the findings identify CP-As and the LIFR signaling pathway as promising targets for future anti-obesity therapies aimed at promoting healthier aging.