Study: Fat tissue of older mice lose the ability to restore body heat in cold temperatures

The evolution of humans has given them a level of protection from the existential risk of cold temperature with the ability to generate heat from fat stored in the body.

Study: Fat tissue of older mice lose the ability to restore body heat in cold temperatures
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But as people age, they become more prone to cold as well as inflammation and metabolic problems that can cause various chronic diseases. Scientists from Yale and the University of California-San Francisco (UCSF) have identified one main reason for this process—the same immune cells containing fat and designed to safeguard humans from cold temperatures.

As part of new research, the researchers identified that in older mice, the fat tissue loses the immune cell group 2 innate lymphoid cells (ILC2) that restore body heat during cold temperatures. However, in a cautionary narrative for those looking for easy treatments for aging-related diseases, they also identified that triggering the production of new ILC2 cells in aging mice makes them more susceptible to cold-induced death.

According to Vishwa Deep Dixit, the Waldemar Von Zedtwitz Professor of Comparative Medicine and of Immunobiology and co-corresponding author of the study, “What is good for you when you are young, can become detrimental to you as you age.”

The findings of the study were published in the Cell Metabolism journal on September 1st, 2021.

Dixit and his former colleague Emily Goldberg, who is now an assistant professor at UCSF, were inquisitive about why fat tissue stores immune system cells that are often concentrated in areas exposed to pathogens, such as skin, nasal passages, and lungs.

The researchers sequenced genes from cells of young and old mice, identifying that older animals lacked ILC2 cells, a lack that restricted their ability to burn fat and increase their body temperature in cold conditions.

Upon introducing a molecule to boosts the synthesis of ILC2 in aging mice, the immune system cells were found to be restored. However, the mice were astonishingly even less tolerant of cold temperatures.

The simple assumption is that if we restore something that is lost, then we are also going to restore life back to normal. But that is not what happened. Instead of expanding healthy cells of youth, the growth factor ended up multiplying the bad ILC2 cells that remained in fat of old mice.”

Vishwa Deep Dixit, Waldemar Von Zedtwitz Professor of Comparative Medicine and Immunobiology, Yale University

However, ILC2 cells from younger mice were transplanted into older mice, the ability of the older animals to tolerate cold was restored.

Immune cells play a role beyond just pathogen defense and help maintain normal metabolic functions of life. With age, the immune system has already changed and we need to be careful how we manipulate it to restore the health of elderly.”

Vishwa Deep Dixit, Waldemar Von Zedtwitz Professor of Comparative Medicine and Immunobiology, Yale University

Source:
Journal reference:

Goldberg, E. L., et al. (2021) IL-33 causes thermogenic failure in aging by expanding dysfunctional adipose ILC2. Cell Metabolism. doi.org/10.1016/j.cmet.2021.08.004.

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