New research shows that immune cells play an unexpected role in regulating body fat. When the body is exposed to cold or other forms of metabolic stress, neutrophils — a common type of immune cell — quickly move into fat tissue and send signals that slow the breakdown of stored fat. Scientists believe this response evolved to prevent humans from losing too much fat during periods of scarcity or long exposure to cold.
In mouse studies, activating the sympathetic nervous system triggered this surge of neutrophils into visceral fat, where they helped limit additional fat loss. When researchers removed either the neutrophils or the signals they release, the animals burned through their fat stores much faster. Human genetic data showed similar patterns, with key genes in this pathway more active in people with obesity, suggesting the system may behave differently depending on someone’s metabolic state.
The findings reveal a new connection between the immune system and fat tissue. By influencing how quickly stored fat is used, immune cells appear to play a much larger role in energy balance than previously understood. This pathway may lead to future treatments for obesity, metabolic syndrome and conditions that cause unintended weight loss.
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