Immune System Blocks Weight Loss: UC San Diego Study Links Neutrophils to Obesity
- 14 dic
- 2 Min. de lectura
A groundbreaking study from the University of California San Diego School of Medicine has unveiled an unexpected collaboration between the body's defenses and its energy stores, demonstrating a surprising new function for immune cells: actively preventing excess weight loss. Published in Nature, the research reveals a biological mechanism by which the Immune System steps in to slow fat burning, a finding that has profound implications for understanding and treating Obesity.
The central players in this newly discovered defense mechanism are neutrophils, a type of white blood cell. Researchers found that when the body is subjected to physiological stress—such as exposure to low temperature or periods of fasting—these neutrophils infiltrate white adipose tissue (WAT), commonly known as body fat. WAT is crucial for energy balance, storing and releasing energy as needed during metabolic stress. Upon arrival in the fat tissue, the neutrophils release signaling molecules that actively suppress further fat loss in the surrounding tissue.
This mechanism appears to be a biological safeguard, perhaps developed in early human ancestors to preserve vital energy stores when food was scarce or during prolonged cold. Crucially, the researchers observed that when these signaling molecules or the neutrophils themselves were depleted in mouse models, the mice experienced increased fat breakdown under metabolic stress. Moreover, in obese individuals, the genes associated with this specific immune pathway were found to be more active, suggesting this protective fat-preserving response may exacerbate the challenges of Obesity today.
This discovery reframes the immune system not only as a defender against infection but also as a crucial regulator of energy balance.
The findings build upon a broader understanding of the relationship between metabolic health and the Immune System. Obesity itself is characterized as a chronic, low-grade inflammatory disorder, often referred to as "meta-inflammation". In individuals with obesity, there are increased numbers of immune cells, including lymphocytes, monocytes, and neutrophils, and increased production of pro-inflammatory cytokines like TNFα and IL-6, both systemically and locally within the adipose tissue.
However, evidence consistently shows that sustained weight loss—whether achieved through lifestyle modifications, pharmacological therapies, or surgical procedures like gastric bypass (RYGB) and sleeve gastrectomy (VSG)—reduces this burden of inflammation. Weight loss reduces overall white blood cell (WBC) and lymphocyte counts and consistently lowers key inflammatory biomarkers such as C-reactive protein (CRP) and IL-6.
By identifying the precise immune pathway that stalls fat breakdown, the UC San Diego study provides a compelling new target. Targeting this neutrophil-mediated pathway may ultimately offer innovative strategies for treating Obesity, metabolic syndrome, and conditions involving unintended weight loss. This research transforms how we view the battle of the bulge: it’s not just metabolism fighting food intake, but the Immune System fighting to maintain fat reserves. If the body’s natural defense mechanism acts like a stubborn anchor on the scales, unlocking this pathway could finally allow for smoother sailing toward effective weight loss.
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Keywords: Immune System Blocks Weight Loss
Immune System Blocks Weight Loss
