The same white blood cells that rush to fight infection seem to have a second job: preventing your body from burning too much fat.
Researchers at UC San Diego School of Medicine set out to understand how the body prevents excessive fat loss during periods of stress, such as cold exposure or fasting. They knew immune cells change in response to overeating and obesity but wondered what happens on the other side of the equation.
They used a drug to pharmacologically activate the same pathway that cold exposure would trigger in mice. Within hours of the stress signal, neutrophils — immune cells typically associated with fighting bacteria — flooded into visceral fat, the fat surrounding vital organs. Once there, the neutrophils released interleukin-1-beta (IL-1-beta), a signalling molecule that tells fat cells to slow down lipolysis, the process of breaking down stored fat to release energy.
From an evolutionary standpoint, this braking mechanism makes sense. When our ancestors faced prolonged cold or food scarcity, burning through fat reserves too quickly could be fatal. The body needed a way to pace itself.
However, insulin normally suppresses lipolysis after eating — when the body has fresh fuel and doesn’t need to tap fat reserves – but when cells become resistant to insulin, that brake weakens, leading to chronically elevated fatty acid release, increased neutrophil recruitment, and more inflammation.
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