By identifying the molecular cause of age-related abdominal fat, a team of US researchers has shed light on why our midsections enlarge as we age.

The results, which were published in the journal Science, point to a new target for treatments in the future that will help us avoid belly fat and live longer, healthier lives.

This study was conducted via preclinical research by City of Hope, one of the biggest and most cutting-edge cancer research and treatment institutions in the United States.

According to Qiong (Annabel) Wang, an associate professor of molecular and cellular endocrinology at the Arthur Riggs Diabetes and Metabolism Research Institute at City of Hope, “people often lose muscle and gain body fat as they age — even when their body weight remains the same.”

“We found that ageing promotes the body’s massive production of new fat cells, particularly around the belly, and triggers the arrival of a new type of adult stem cell,” Wang said.

Together with co-corresponding author Xia Yang from the UCLA group, the researchers carried out a number of animal tests that were subsequently confirmed on human cells.

White adipose tissue (WAT), the fatty tissue that causes age-related weight increase, was the focus of Wang and her colleagues’ investigation.

Although it is well known that fat cells enlarge with age, the scientists hypothesised that WAT also grew by generating new fat cells, suggesting that it may have limitless growth potential.

The researchers employed adipocyte progenitor cells (APCs), a subset of stem cells in WAT that develop into fat cells, to test their theory.

APCs from young and elderly mice were initially transplanted into a second set of young mice by the scientists. The elder animals’ APCs produced an enormous number of fat cells very quickly.

However, the stem cells did not produce many new fat cells when the scientists transplanted APCs from young mice into the older animals. The findings demonstrated that older APCs, irrespective of the age of their host, are capable of producing new fat cells on their own.

The researchers next contrasted the activity of the APC gene in young and aged mice using single-cell RNA sequencing. APCs sprang up with a fury in middle-aged mice and started pumping out new fat cells, while they were hardly active in young mice.

Leukaemia inhibitory factor receptor (LIFR), a signalling pathway, was shown to be essential for encouraging the proliferation and transformation of these CP-A cells into fat cells.

We found that LIFR drives the body’s fat-making process. Wang clarified that older mice need this signal to produce fat, whereas younger mice do not. “Our findings suggest that in older mice, LIFR is essential in inducing CP-As to produce new fat cells and increase abdominal fat.”

In order to combat age-related obesity, Wang said, “Our findings highlight the importance of controlling new fat-cell formation.”