Kenneth Glad
Scientists continue to uncover how the body changes over time and what those shifts may mean for long-term health. New findings are offering fresh clues that could guide future medical research.
A newly identified population of fat-cell precursors may help explain why abdominal fat becomes more common with age, according to research covered by ScienceDaily.
City of Hope researchers detected the cells as mice reached middle age. Known as committed preadipocytes, age-specific, or CP-As, they showed an unusual capacity to develop into new fat cells.
That distinction matters because fat tissue can expand in two ways. Existing cells may grow larger, or precursor cells may create additional ones. The study suggests that aging may accelerate the second process around the abdomen.
“People often lose muscle and gain body fat as they age — even when their body weight remains the same,” said Qiong Annabel Wang, an associate professor of molecular and cellular endocrinology at City of Hope. “We discovered aging triggers the arrival of a new type of adult stem cell and enhances the body’s massive production of new fat cells, especially around the belly.”
Transplants revealed the difference
To determine whether the change came from the cells themselves or from their surroundings, the scientists transplanted adipocyte progenitor cells, known as APCs, between mice of different ages.
Older APCs produced many new fat cells after being placed in young animals. Young APCs, by contrast, remained comparatively inactive when transferred into older mice.
According to the study, that result indicated that aging had altered the progenitor cells internally. The surrounding tissue alone did not appear to account for their stronger fat-forming behavior.
Single-cell RNA sequencing later allowed the team to examine activity in individual cells. The analysis showed that progenitor cells were relatively quiet in younger mice but became more active by middle age, when the CP-A population emerged.
A possible biological switch
The researchers also examined the signals directing this process. They identified the leukemia inhibitory factor receptor, or LIFR, pathway as an important part of CP-A growth and development.
Older mice appeared to rely on this signal to produce new fat cells, while younger animals did not show the same dependence. That finding raises the possibility that LIFR could eventually become a therapeutic target, although no treatment has yet been established.
The team then searched for a similar pattern in human tissue. It found CP-A-like cells in greater numbers in samples from middle-aged individuals, and those cells also showed a strong capacity to become fat cells.
The next question is whether targeting this age-related cell population can safely reduce abdominal fat. Further animal studies and human research will be needed before that possibility can be tested clinically.
Sources: ScienceDaily
