Researchers have shown that obesity in experimental models led to senescence of macrophages, an immune cell subtype within fat or adipose tissue.
Many of the macrophages within obese tissue were senescent and those senescent cells may be a significant driver of fat tissue fibrosis. These findings suggest that obesity accelerates cellular or biological immune aging in fat.
“In healthy individuals, those cells contribute to cleaning the tissue from dead cells specialized for the storage of fat called adipocytes and help in the cellular turnover. We demonstrated that macrophages lose this capacity when they become senescent,” explained first and co-corresponding author Nabil Rabhi.
The researchers also found that senescent macrophages secrete a variety of factors, one of which is a molecule called osteopontin which they found is responsible for adipose tissue fibrosis. “Our finding suggests that macrophages age faster in obese animals. This accelerated senescence may contribute to the pathological thickness or fibrosis of fat tissue observed in obese individuals with type 2 diabetes,” said Rabhi.
“Our finding indicates that targeting the senescent macrophages population or using osteopontin inhibition may represent a promising approach for obesity treatment and its adverse complication including type 2 diabetes,” added Rabhi.
Sources:
Nabil Rabhi, Kathleen Desevin, Anna C Belkina, Andrew Tilston-Lunel, Xaralabos Varelas, Matthew D Layne, Stephen R Farmer. Obesity-induced senescent macrophages activate a fibrotic transcriptional program in adipocyte progenitors. Life Science Alliance, 2022; 5 (5): e202101286 DOI: 10.26508/lsa.202101286
Boston University School of Medicine. “Obesity: What does immunity have to do with it? New findings may represent a promising approach for obesity treatment and its complications.” ScienceDaily. ScienceDaily, 22 February 2022. <www.sciencedaily.com/releases/2022/02/220222121240.htm>.
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