By Franklin Delgado
Research led by the University of Birmingham (United Kingdom), published in EMBO Reportsreveals that obesity causes a DNA methylation process in immune cells, which leaves lasting marks on them. These alterations can persist up to ten years after losing weight, maintaining a high risk of obesity-related diseases.
Changes in the immune system affect essential functions such as eliminating waste and regulating aging. It is concluded that, despite weight loss, obese people may still be at risk of type 2 diabetes and cancer.
“Our findings show that obesity is associated with long-lasting epigenetic modifications that influence the behavior of immune cells. This suggests that the immune system retains a molecular record of past metabolic exposures, which may have implications for disease risk and long-term recovery,” said study lead author Belinda Nedjai of the Wolfson Institute of Population Health at Queen Mary University of London. EFE Health.
Study design and results
The study analyzed immune cells from several groups, including obese patients and those on exercise regimens.
Mouse models and blood from healthy volunteers were used to understand the underlying cellular mechanism and its health implications.
Towards new therapies and treatments
The study suggests that ongoing weight management is mandatory to reduce “obesity memory.”
Early intervention in obesity can modify DNA methylation patterns that would otherwise tend to be maintained and favor an unfavorable metabolic state later in life. In simple terms, acting sooner can help “reprogram” the expression of genes related to inflammation, lipid metabolism and mitochondrial function, thus reducing the future risk of diabetes, cardiovascular disease and other metabolic complications.
Investigation of existing drugs, such as SGLT2 inhibitors, is proposed to improve immune function and reduce the risk of metabolic diseases in those who have been obese.
Memory in fat cells
Research published in Nature (2024) show that adipose cells retain epigenetic and transcriptional changes detected by single-nucleus RNA sequencing, promoting weight recovery. These marks persist in human and mouse adipose tissue, making permanent loss difficult.
Therapeutic advances
SGLT2 inhibitors (repurposed from diabetes) are being explored to reduce inflammation and eliminate senescent cells, combined with weight loss therapies. Furthermore, epigenetic editing and drugs such as semaglutide or tirzepatide could attenuate this memory, although direct modifications are not yet available.
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