Feb. 22 (UPI) -- Researchers from Lund University in Sweden have identified changes in DNA methylation that may be linked to the causes of obesity.
DNA methylation is an epigenetic process where small molecules, known as methyl groups, are added to genes to fine-tune gene activity. Epigenetic changes affect the formation of new muscle cells and may be a contributing factor to reduced muscle mass and impaired metabolism found in obesity.
The study, led by Cajsa Davegardh, a doctoral student at Lund University, compared DNA methylation in muscle stem cells in obese and non-obese people.
"Many genes that had changed their genetic expression also changed their degree of methylation during the development to mature muscle cells, which indicates a connection," Davegardh said in a press release.
Results showed the pro-inflammatory gene IL-32 played a vital role in gene maturation and insulin sensitivity in fully mature muscle cells. Impairment of insulin sensitivity is common in obesity and type 2 diabetes.
"By reducing the gene expression, the muscle's insulin sensitivity was increased," Davegardh said.
Researchers compared the differences in DNA methylation in muscle stem cells from obese individuals and normal weight individuals and found partly different genes were regulated during the maturation process and methylation changes were more common in people who were obese than those who were not obese.
"We believe that in obese individuals the muscle stem cells have been reprogrammed, and that this may partly explain why muscle cells in obese people have decreased insulin sensitivity and lower metabolism after they have matured," Davegardh said. "They may also have a protective function. Furthermore, we don't know what happens when you lose weight -- whether the methylations are restored. This would be interesting to follow up."
The study was published in BMC Medicine.