SHAFAQNA – The findings could lead to new methods of obesity prevention, and could even help ward off obesity-related diseases in humans, Weill Cornell Medical School reported.“Understanding how the immune system regulates metabolism and the function of adipose tissue will help guide investigations into immune-based therapies to limit fat accumulation,” he says. “Of course, a lot more work is needed before we get there, but this study provides significant insights into this pathway.”
The researchers discovered a subset of immune cells, dubbed group 2 innate lymphoid cells (ILC2s) that allow fat tissue to take on a metabolically active state that helps burn calories. The phenomenon occurs when a specialized fat-burning cell type called the “beige” fat cell is activated.
To make their findings the researchers looked at white fat in both obsess and non-obsese participants and found decreased levels of ILC2s in obese white adipose tissue.Past studies have found mice that did not have normal ILC2s tended to become obese and even showed early signs of diabetes.
“Our studies indicate that ILC2s have beneficial effects that decrease obesity and suggest that boosting ILC2s in fat should be explored as a potential therapeutic strategy to treat obesity,” said Jonathan Brestoff, a Perelman School of Medicine MD-PhD student in the Artis lab who performed the studies.
The findings also suggest immune control of fat tissue is an evolutionary response to stress imposed on the body.
“For example, imagine that a person infected with the flu is sick, feverish and has no appetite. One can envision the value in reprogramming metabolic processes – such as holding on to stores of body fat – to help the body get through this stressful period associated with infection,” Brestoff said.
ILC2 regulation of fat storage may have evolved to adapt to changes in food abundances, such as in times of famine. It may have eventually become defective, disconnecting the immune system from metabolic pathways.
The findings were published in a recent edition of the journal Nature.
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