Why does fat tend to settle around the middle as we get older? Researchers at the California research center City of Hope, with collaborators at UCLA, report that they have found a likely culprit: a distinct group of fat-cell precursors that emerges with age and preferentially builds new fat in the abdomen, according to a summary of the study.
A new kind of fat precursor
The team calls the cells "committed preadipocytes, age-specific," or CP-As. In experiments published in the journal Science, they found these cells are largely absent in young animals but accumulate in the abdominal fat of older mice. When progenitor cells from older mice were transplanted into younger ones, they generated far more new fat cells than young progenitors did — pointing to the cells themselves, rather than their surroundings, as the driver.
How it appears to work
At the molecular level, the researchers implicate a signaling receptor called LIFR (leukemia inhibitory factor receptor). "Our research indicates that LIFR plays a crucial role in triggering CP-As to create new fat cells and expand belly fat in older mice," said co-corresponding author Qiong (Annabel) Wang. Notably, young mice did not appear to need this signal to make fat cells, while older mice did — suggesting the pathway becomes specifically coupled to fat production with age.
Mice first — then a look at human tissue
It is worth being precise about what was shown. The core experiments were done in mice. The researchers then used single-cell sequencing on human fat-tissue samples and found cells resembling CP-As, more abundant in samples from middle-aged donors. That cross-species comparison is suggestive, but the study did not track these cells in living people or test whether blocking LIFR reduces fat in humans. It establishes a correlation, not a confirmed human mechanism.
Why it matters
Abdominal, or visceral, fat is metabolically different from fat stored elsewhere and is more strongly linked to heart disease, insulin resistance and some cancers. Understanding why it accumulates specifically in midlife has been a long-standing puzzle — made more curious by earlier findings that fat-cell turnover generally slows with age. The team's answer is that a small but potent group of precursors becomes activated, rather than the whole pool speeding up.
Early days
The researchers frame the work as a foundation, not an imminent treatment. No drug targeting LIFR or CP-A cells in age-related fat has entered clinical trials, and scientists routinely caution that the road from a mechanism in mice to a proven human therapy is long and often fails. Still, the study offers a specific cellular and molecular target where none existed before — a meaningful step toward understanding why the body's shape shifts so predictably with the years.
