It is no secret that our waists often expand in the middle age, but the problem is not strictly cosmetic. The belly fat accelerates aging and slows metabolism, increasing our risk of developing diabetes, heart problems and other chronic diseases. However, age is exactly a package of six into a softer stomach is cloudy.
Now preclinical research of the city of hope®One of the largest and most advanced cancer research and treatment organizations in the United States and a leading diabetes research center and other diseases that threaten life, have discovered the guilty cell behind abdominal fat related to age, providing new ideas about why our medium directions are extended with the Middle Ages. Posted today in ScienceThe findings suggest a novel goal for future therapies to prevent the sagging of the belly and extend our healthy useful life.
“People often lose muscle and gain body fat as they age, even when their body weight remains the same,” Saidqiong (Annabel) Wang, Ph.D., author of the corresponding study of the study and associate profess from the city of the city of Hope, and the Metabolism Research Institute of the world dedicated to the Bosigates organizations of the Biology Bible dedicated to the Bible Bible of the Bible Bible Bible and the treatment of the Riggs of the Bible Bible of the Bible Bible of the Bible Bible of the Bible Bible of the Bible Bible of the Bible of the Bible of the Bible of the Bible of the Bible of the Bible Bible Bosigrations. diabetes. “We discover that aging triggers the arrival of a new type of adult stem cells and improves the massive production of the body of new fatty cells, especially around the belly.”
In collaboration with the co-corrected author of the Laboratory of the UCLA, Xia Yang, Ph.D., the scientists conducted a series of mouse experiments later validated in human cells. Wang and his colleagues focused on the white adipose tissue (WAT), the fatty tissue responsible for age -related weight gain.
While it is well known that fatty cells grow with age, scientists suspected that Wat also expanded by producing new fat cells, which means that it can have unlimited potential to grow.
To test their hypothesis, the researchers focused on Adipocyte’s progenitor cells (APC), a group of stem cells in Wat that evolve in fatty cells.
The team of the city of Hope first transplanted the APC of young mice and older to a second group of young mice. The APC of the oldest animals quickly generated a colossal amount of fat cells.
However, when the team transplanted the APC of young mice to the oldest mice, stem cells did not manufacture many new fatty cells. The results confirmed that the oldest APCs are equipped to make new fatty cells independently, regardless of the age of their host.
Using single -cell RNA sequencing, scientists compared the APC gene activity in young and old. Although just active in young mice, APC woke up with revenge in middle -aged mice and began pumping new fatty cells.
“While the ability of most adult stem cells to cultivate floors with age, the opposite is true with the APCs: aging unlocks the power of these cells to evolve and spread,” said Adolfo Garcia-Ocana, Ph.D., Ruth B. and Robert K. Lanman, the president of gene regulation and discovery of drugs and president of the Department of Molecular and Cellular Department In the city of the city of Hope de Hope. “This is the first evidence that our bellies expand with age due to the high APC production of new fatty cells.”
Aging also transformed APCs into a new type of stem cells called compromised preadipocytes, specific (CP-AS). As CP-A cells actively produce new fat cells, explaining why major mice gain more weight.
A signaling route called Inhibitory Factor of Leukemia Factor (LIFR) proved to be critical to promote these CP-A cells to multiply and evolve into fatty cells.
“We discovered that the body’s fat manufacturing process is driven by LIFR. While young mice do not require this sign to make fat, major mice do it,” Wang explained. “Our research indicates that LIFR plays a crucial role in the trigger of CP-as to create new fatty cells and expand the abdominal fat in major mice.”
Using the Single Cell RNA sequencing in samples of people of various ages, Wang and their colleagues then studied APC of human fabric in the laboratory. Again, the team also identified similar CP-A cells that had a larger number in the fabric of medium-sized people. His discovery also illustrates that CP-as in humans has high capacity to create new fatty cells.
“Our findings highlight the importance of controlling the new formation of fatty cells to address age-related obesity,” Wang said. “Understanding the role of CP-as in metabolic disorders and how these cells arise during aging could lead to new medical solutions to reduce belly fat and improve health and longevity.”
Future research will focus on tracing CP-A cells on animal models, observe CP-A cells in humans and develop new strategies that eliminate or block cells to prevent age-related fat gain.
The first authors of the study are Guan Wang of City of Hope, Ph.D., and Gaoyan Li de UCLA, Ph.D.