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In a new study from the University of Minnesota, researchers found there are numerous areas of the genome where obese and non-obese individuals differ in terms of their “methylome.”
Essentially, the researchers found that the level of DNA methylation (addition or subtraction of a methyl group on the DNA molecule) was related to level of body mass index (BMI), a marker of obesity. These differences in methylome are a type of “epigenetic” variation, which does not involve the genetic sequence itself, but rather is thought to alter which genes are turned “on” and “off” at a given point in time in a given tissue. Typical genetic sequences do differ but data shows these differences go beyond that.
Lead author, Ellen Demerath, Ph.D., associate professor of epidemiology and community health at University of Minnesota’s School of Public Health conducted the study in collaboration with other U of M researchers and researchers at three other United States institutions all of whom are working on the large on-going Atherosclerosis Risk in Communities (ARIC) Study. This is a 30-year prospective study of coronary heart disease risks in both white and African American adults ages 45-55 when the study started in 1985.
“Study participants are tracked annually and also brought in for blood draws and detailed examinations. This includes the measurement of body mass index (BMI) and waist circumference, typical markers of obesity,” said Demerath.
Researchers found these differences were not only noted in the blood but in fat tissue DNA as well. This could provide useful information about methylation in other disease-relevant tissues that are typically difficult to collect in large-scale community based studies.
When comparing their results for over 2,000 African American individuals with 3,000 white individuals in other studies, researchers were interested to learn signatures of obesity were largely similar across race/ethnic groups.
“This has not been shown before. It supports the idea that many of the same molecular pathways disrupted in obesity probably operating in both African Americans and Whites,” said Demerath.
The team’s goal of this research and other epigenetic research is to get a more exact understanding of how the behavioral factors including obesity, exercise, and cigarette smoking, as well as environmental exposures such as air pollution and dietary factors can change the DNA over our lifetime, and lead to disease.
“The results will hopefully be followed up with longitudinal data to assess whether these DNA methylation changes in obese individuals are permanent, or are changed if they lose weight,” said Demerath. “The work is exciting because it might be possible to design pharmaceutical or dietary or other behavioral interventions that specifically target these epigenetic signatures to avert diabetes and coronary heart disease.”
Demerath and her colleagues are submitting a number of NIH grant proposals this year to continue their research and expand its scope to look at methylation changes over time, race differences and genetic determinants of methylation variation related to obesity and diabetes.
“We want to achieve a very comprehensive understanding of the role of epigenetics in chronic disease in African Americans, and the ARIC study is fortunate to have one of the larger samples of African Americans of any epigenetic study in the United States,” said Demerath.
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