From the median age we usually tend to accumulate body fat in certain areas and our waist widens, a problem that goes beyond aesthetics, since abdominal fat helps to slow down metabolism and the development of chronic diseases such as diabetes, or cardiovascular disorders.
Until now it was not known why aging influences so that a firm abdomen becomes fofo and soft, but a new study conducted by City of Hope experts has identified the culprit at the cellular level of the appearance of abdominal fat related to age, which provides new knowledge about why the middle areas of the body widen with the median age.
The results of their work have been published in Science and suggest a new goal to design future therapies that help prevent abdominal sagging and to prolong our healthy life expectancy. “People often lose muscle mass and gain body fat as they age, even when their body weight remains the same,” said Qiong (Annabel) Wang, corresponding co -author of the study and associate professor of molecular and cellular endocrinology at the Arthur Riggs Diabetes and Metabolism Institute of City of Hope in a note published by the center. “We discover that aging triggers the arrival of a new type of adult stem cell and improves the mass production of new fatty cells in the body, especially around the abdomen,” he adds.
A new approach to age -related obesity
In collaboration with Dr. Xia Yang, co -author of the UCLA laboratory, scientists conducted a series of experiments with mice that subsequently validated with human cells. The researchers focused on the white adipose tissue (tab), the fatty tissue responsible for age -related weight gain.
Although it was already known that fatty cells increased with age, scientists suspected that white adipose tissue also expanded producing new fatty cells, which means that it could have unlimited potential to grow. To test their hypothesis, they focused on the progenitor cells of the adipocytes (CPA), a group of white adipose tissue stem cells that evolve until they become fatty cells.
The City of Hope team first transplanted adipose stem cells (CMA) of young mice and older to a second group of young mice. The CMA of major animals quickly generated a colossal amount of adipose cells. However, when the team transplanted adipose stem cells (CMA) of young mice to major mice, stem cells did not produce many new adipheose cells. The results confirmed that the highest CMAs are trained to produce new adipose cells independently, regardless of the age of their host.
“This is the first evidence that our bellies expand with age due to the high production of new fat cells by adipose stem cells”
Through the sequencing of unicellular RNA, scientists compared the activity of the APC gene in young and old mice. While they were barely activated in young mice, APCs were strongly reactivated in medium -sized mice and began producing new fatty cells. “While the growth capacity of most adult stem cells decreases with age, the opposite occurs with the CMA: aging releases its ability to evolve and spread,” said Adolfo García-Acaña, head of the Ruth B. & Robert K. Lanman chair in gene regulation and discovery of discovery of drugs and director of the Department of Molecular and Cellular Endocrinology of Molecular and Cellular. “This is the first evidence that our bellies expand with age due to the high production of new fat cells by CMA.”
Aging also transformed adipheose stem cells (CMA) into a new type of stem cell called compromised preadipocytesSpecific age (CP-A). As CP-A cells actively produce new fat cells, which explains why major mice gain more weight. A signaling route called the leukemia inhibitor factor (LIFR) was essential to promote that these CP-A cells multiply and evolve until they become fat cells.
“We discover that the body fat production process is driven by LIFR. While young mice do not require this signal to produce fat, major mice do need it,” Wang explained. “Our research indicates that LIFR plays a crucial role in the activation of CP-A to create new fat cells and expand abdominal fat in major mice.”
Through the sequencing of unicellular RNA in samples of people of various ages, Wang and their colleagues subsequently studied the adenomatous stem cells (CMA) of human tissue in the laboratory. The team also identified similar CP-A cells, whose number increased in the fabric of middle-aged people. Its discovery also illustrates that CP-A in humans have a high capacity to create new fatty cells.
“Our findings highlight the importance of controlling new fatty cells to address obesity related to age,” said Wang. “Understanding the role of CP-A in metabolic disorders and how these cells arise during aging could lead to new medical solutions to reduce abdominal fat and improve health and longevity“.
Future investigations will focus on monitoring CP-A cells on animal models, the observation of CP-A cells in humans and the development of new strategies that eliminate or block cells to prevent the increase in fat related to age.
Source: www.webconsultas.com