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Obesity is a serious global health crisis, and it may leave a lasting imprint on the immune system that keeps people at risk for obesity-related conditions, even years after losing weight. New research indicates that obesity may leave T cells in a prolonged pro-inflammatory state, even after normal weight is regained
Under healthy conditions, abdominal adipose tissue is populated by anti-inflammatory immune cells, particularly regulatory T cells, that regulate inflammatory responses. In obesity, this immune landscape shifts toward pro-inflammatory cell populations, resulting in chronic low-grade inflammation that drives metabolic dysfunction and disease.
The researchers modeled obesity by feeding female mice different diets for 14 weeks, then switched them to a normal diet for six weeks to promote recovery. Although adipose tissue mass fully normalized, indicating restoration of metabolic balance, the pro-inflammatory effector memory response persisted.
DNA methylation, a process in which chemical markers are added to DNA in immune cells, may leave lasting biological changes that persist for five to ten years after weight loss. This enduring “memory” of obesity in helper T cells could contribute to dysregulation of normal immune system activity.
The research concluded that even after reaching a healthy weight, lingering low-grade inflammation may continue to increase the risk of obesity-related conditions, including metabolic syndrome and cardiovascular disease. Managing obesity is a long-term process rather than a quick fix, as the immune system may take years to fully readjust after weight loss.
To view the original scientific study click below:
DNA methylation-mediated memory of obesity in CD4 T lymphocytes perpetuates immune dysregulation
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