What Cellular Mechanism Is Behind Age-Related Abdominal Fat?

New York, April 27 (NationPress) A group of researchers from the United States has identified the cellular mechanism responsible for the accumulation of abdominal fat as we age, shedding light on why our waistlines expand during middle age.

Published in the journal Science, the research presents a promising target for future interventions aimed at preventing belly fat and enhancing our quality of life as we age.

This preclinical study was conducted by City of Hope, recognized as one of the largest and most advanced institutions for cancer research and treatment in the United States.

“As people age, they often experience muscle loss and an increase in body fat, even if their overall weight remains stable,” remarked Qiong (Annabel) Wang, an associate professor of molecular and cellular endocrinology at City of Hope’s Arthur Riggs Diabetes and Metabolism Research Institute.

“Our discovery shows that aging triggers the emergence of a new type of adult stem cell, significantly boosting the body's production of new fat cells, particularly around the abdomen,” Wang added.

In collaboration with Xia Yang from UCLA, the researchers conducted a series of experiments on mice, which were later confirmed using human cells.

Wang and her team focused on white adipose tissue (WAT), the fatty tissue that contributes to weight gain associated with aging.

While it is widely acknowledged that fat cells increase in size with age, the researchers hypothesized that WAT also grows by generating new fat cells, suggesting it may have an unlimited capacity for expansion.

To validate their hypothesis, the team examined adipocyte progenitor cells (APCs), a subset of stem cells in WAT that differentiate into fat cells.

They transplanted APCs from both young and older mice into a new set of young mice, discovering that the APCs from older mice rapidly produced an enormous number of fat cells.

In contrast, when they transplanted APCs from young mice into older mice, the stem cells failed to generate many new fat cells. These results confirmed that older APCs possess the capability to independently produce new fat cells, regardless of the age of their host.

Using single-cell RNA sequencing, the scientists compared APC gene activity between young and older mice. While APCs were largely inactive in young mice, they became highly active in middle-aged mice, leading to a surge in new fat cell production.

A significant signaling pathway known as the leukemia inhibitory factor receptor (LIFR) was found to be essential for the proliferation of these CP-A cells into fat cells.

“Our research indicates that the fat production process is regulated by LIFR. Young mice do not require this signal to generate fat, but older mice do,” Wang explained. “These findings underline the critical role of LIFR in prompting CP-As to form new fat cells and increase belly fat in older mice.”

“Our results emphasize the necessity of regulating new fat cell formation to combat age-related obesity,” Wang concluded.