Scientists say chemical changes to 13 human genes may be tied to obesity.
Such chemical changes, known as epigenetic changes, don’t alter the genes’ DNA sequence, but alter the way that sequence is read by cells.
A study published today (Sept. 15) found a relationship between a person’s body mass index and changes to 13 genes that were already suspected of having a role in obesity. The changes consist of DNA methylation — the addition of a certain chemical “tag” to a section of DNA that prevents genes from being expressed.
The findings could have implications for personalized medicine, the idea that health care and treatments can be tailored to an individual’s unique body and genetic information. If certain genes or epigenetic changes are found to increase one’s risk of obesity, individuals with these genetic traits would be aware of the danger and could try altering their diet and exercise habits or taking medications.
“In trying to identify what might be different from one person to another that might have health relevance, we can and should do epigenetic profiling,” said study author Andrew Feinberg, director of the Center for Epigenetics at Johns Hopkins University in Baltimore.
Future research should focus on the 13 identified genes to see if they are in fact related to obesity, or to other diseases tied to body mass index, such as diabetes, Feinberg told MyHealthNewsDaily.
The study appears in today’s issue of the journal Science Translational Medicine.
Feinberg and his colleagues scanned the genetic information of 74 people from Iceland, using DNA samples taken in 1991 and 2002. Specifically, the researchers were looking for areas of the DNA strand that varied between individuals in terms of how many genes underwent DNA methylation. They found 227 such regions.
Because many genes have the same methylation pattern from person to person, the researchers said the methylation of these 227 regions basically represents an epigenetic “fingerprint” unique to each person.
The results also showed that these fingerprints, for the most part, remained relatively stable in each person over the 11-year period. About two-thirds of the 227 regions did not change considerably over that time, which indicated that the fingerprints are a lasting part of a person’s cell chemistry, not just a fleeting chemical blip.
The researchers then looked to see whether these fingerprints were related to body mass, and found 13 regions in which they were. These 13 regions were on or near genes previously suspected of playing a role in obesity and diabetes, the researchers said.
These chemical tags that determine someone’s fingerprint could be due to environmental influences, the researchers said. Or they could also have their root in genes — in other words, there could be some underlying genetic code that determines how much tagging occurs and where it happens.
Feinberg suspects it’s a little bit of both. Studies on younger individuals, on whom the influence of the environment may be more limited, might provide an answer.
Future research should also be done on larger, more diverse populations to validate and add to the findings.
The study was funded by the National Institute of Environmental Health Sciences, the National Human Genome Research Institute and the National Institute on Aging, all of the United States, and the Icelandic Heart Association and the Icelandic Parliament.