Molecular biologists have discovered that obesity causes long-lasting changes in the set of markers on the surface of DNA in immune system cells.
This affects the activity of a large number of genes and persists long after weight returns to normal, according to a press release from the University of Birmingham.
The university's press service quoted Professor Claudio Mauro of the University of Birmingham as saying: "This finding suggests that short-term weight loss does not reduce the risk of developing many obesity-related diseases, such as type 2 diabetes or some types of cancer. It appears that a person needs to maintain a normal weight for at least 5-10 years for this obesity-related 'memory' to disappear."
Biologists reached this conclusion while studying the changes caused by obesity in the structure of T-cell genomes and other components of the immune system. Recent experiments have shown that obesity makes these cells more susceptible to developing inflammation because excess weight specifically alters the structure and distribution of certain markers on the DNA surface that affect gene activity.
These observations prompted biologists to investigate how weight loss affects gene function in T cells. To gather this information, researchers raised several groups of mice, feeding some a high-calorie diet until the rodents became obese, then switching them to a normal-calorie diet. Simultaneously, the researchers collected T cell samples from the animals and monitored changes in their genome function.
Analysis by biologists showed that the T cells of mice that lost weight continued to produce signaling molecules that contribute to inflammation for several weeks after weight loss, suggesting a long-term "molecular memory" of obesity in their immune cells. Researchers reached similar conclusions when analyzing blood samples from volunteers who had recently lost excess weight, as well as from carriers of rare genetic disorders that increase the risk of obesity.
Scientists noted that the strongest changes were recorded in genes associated with cellular "waste" processing and T-cell aging.
In the future, this information may enable the development of methods that normalize the function of these regions of DNA and make T cells and other components of the immune system less prone to developing inflammation in the bodies of patients who are still obese or who have recently lost excess weight.
