01.07.21
A new animal study, published in the journal Nature Metabolism and conducted by researchers at UT Southwestern Medical Center, has identified and implicated a specific type of cell lining blood vessels which appears to have a prominent role in obesity-related chronic inflammation.
At least in mice, a type of cell called the adipose progenitor cell, which goes on to generate mature fat cells, was discovered in 2018. The present study found that unlike most APCs, these newly-discovered cells – dubbed fibro-inflammatory progenitors (FIPs) – produced signals that encouraged inflammation.
“The inflammation of fat cells in obese individuals is linked to many of the comorbidities we associate with being overweight – cancer, diabetes, heart disease, and infection,” study leader Rana Gupta, PhD, associate professor of internal medicine, said. “By identifying these cells, we’ve taken a step toward understanding some of the initial events that could contribute to that inflammation.”
The mechanism by which inflammation occurs in white adipose tissue (WAT) among obese people is not well-understood. To this point, it’s known that fat cells begin to die in obesity, triggering an inflammatory immune response. Previous research focused on signaling molecules produced by the fat cells or immune cells in WAT that might contribute to inflammation. The present study focused instead on the blood vessels that carry immune cells and inflammatory molecules into WAT.
In the animal study, young male mice introduced to a high-fat diet underwent a phenomenon in which their FIPs quickly increased the number of inflammatory molecules produced. A 28-day high-fat diet also caused a substantial increase in the proportion of FIPs compared with other APCs.
“This is the first study to demonstrate that these cells play a very active, early role in being gatekeepers of inflammation in fat tissue,” Gupta said.
Mice which were depleted of a gene in order to prevent FIPs from generating normal inflammatory signals no longer had high levels of inflammation when introduced to the high-fat diet.
Interestingly, Gupta and his colleagues went on to demonstrate that increasing levels of a related signaling molecule, ZFP423, in FIPs can also ameliorate the inflammation in mouse fat cells. The findings point toward possible avenues to pursue to lower the risk of disease in people with obesity. In essence, it could work as a brake for the inflammatory signals normally produced by FIPs.
The study authors intend to conduct further experiments in animal models, as well as human clinical studies which will further elucidate whether the mechanisms work similarly in human fat.
At least in mice, a type of cell called the adipose progenitor cell, which goes on to generate mature fat cells, was discovered in 2018. The present study found that unlike most APCs, these newly-discovered cells – dubbed fibro-inflammatory progenitors (FIPs) – produced signals that encouraged inflammation.
“The inflammation of fat cells in obese individuals is linked to many of the comorbidities we associate with being overweight – cancer, diabetes, heart disease, and infection,” study leader Rana Gupta, PhD, associate professor of internal medicine, said. “By identifying these cells, we’ve taken a step toward understanding some of the initial events that could contribute to that inflammation.”
The mechanism by which inflammation occurs in white adipose tissue (WAT) among obese people is not well-understood. To this point, it’s known that fat cells begin to die in obesity, triggering an inflammatory immune response. Previous research focused on signaling molecules produced by the fat cells or immune cells in WAT that might contribute to inflammation. The present study focused instead on the blood vessels that carry immune cells and inflammatory molecules into WAT.
In the animal study, young male mice introduced to a high-fat diet underwent a phenomenon in which their FIPs quickly increased the number of inflammatory molecules produced. A 28-day high-fat diet also caused a substantial increase in the proportion of FIPs compared with other APCs.
“This is the first study to demonstrate that these cells play a very active, early role in being gatekeepers of inflammation in fat tissue,” Gupta said.
Mice which were depleted of a gene in order to prevent FIPs from generating normal inflammatory signals no longer had high levels of inflammation when introduced to the high-fat diet.
Interestingly, Gupta and his colleagues went on to demonstrate that increasing levels of a related signaling molecule, ZFP423, in FIPs can also ameliorate the inflammation in mouse fat cells. The findings point toward possible avenues to pursue to lower the risk of disease in people with obesity. In essence, it could work as a brake for the inflammatory signals normally produced by FIPs.
The study authors intend to conduct further experiments in animal models, as well as human clinical studies which will further elucidate whether the mechanisms work similarly in human fat.
