New York, April 27 A team of US researchers has uncovered the cellular culprit behind age-related abdominal fat, providing new insights into why our midsections widen with middle age.
Published in the journal Science, the findings suggest a novel target for future therapies to prevent belly flab and extend our healthy lifespans.
Preclinical research by City of Hope, one of the largest and most advanced cancer research and treatment organisations in the US, has done this research.
“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’s Arthur Riggs Diabetes and Metabolism Research Institute.
“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,” Wang added.
In collaboration with the UCLA laboratory co-corresponding author Xia Yang, the scientists conducted a series of mouse experiments later validated on human cells.
Wang and her colleagues focused on white adipose tissue (WAT), the fatty tissue responsible for age-related weight gain.
While it’s well-known that fat cells grow larger with age, the scientists suspected that WAT also expanded by producing new fat cells, meaning it may have an unlimited potential to grow.
To test their hypothesis, the researchers focused on adipocyte progenitor cells (APCs), a group of stem cells in WAT that evolve into fat cells.
The team first transplanted APCs from young and older mice into a second group of young mice. The APCs from the older animals rapidly generated a colossal amount of fat cells.
When the team transplanted APCs from young mice into the older mice, however, the stem cells did not manufacture many new fat cells. The results confirmed that older APCs are equipped to independently make new fat cells, regardless of their host’s age.
Using single-cell RNA sequencing, the scientists next compared APC gene activity in young and older mice. While barely active in young mice, APCs woke up with a vengeance in middle-aged mice and began pumping out new fat cells.
A signalling pathway called leukemia inhibitory factor receptor (LIFR) proved critical for promoting these CP-A cells to multiply and evolve into fat cells.
“We discovered that the body’s fat-making process is driven by LIFR. While young mice don't require this signal to make fat, older mice do,” explained Wang. “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.”
“Our findings highlight the importance of controlling new fat-cell formation to address age-related obesity,” said Wang.
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