Contributors to diabetes identified by epigenome study

A new study has collected several clues that indicate how diabetes is triggered by genes and the environment uniting.
These clues were found during a study of genomes, an organism’s complete set of DNA and epigenomes, chemical tags on DNA which control the genome. They were tested on lean and obese mice and humans.
The study was conducted by scientists at the Centre for Epigenetics in the Institute for Basic Biomedical Sciences at the Johns Hopkins University School of Medicine.
They sought to examine the epigenetics of mice who were otherwise identical, but fed either normal or high-calorie diets.
Clear differences were found between the normal and obese mice, with epigenetic marks analysed at more than seven million sites in the DNA of fat cells in the mice.
Methyl groups, which prevent genes from making proteins, were absent in different sites of the lean and obese mice, with research into this pattern of difference in humans providing similar results.
Risk of diabetes
The scientists concluded that obesity-induced changes to the epigenome are similar between mice and humans. “This study yielded a list of genes that previously have not been shown to play a role in diabetes,” said G. William Wong, PhD, associate professor of physiology in the Centre for Metabolism and Obesity Research at Johns Hopkins.
Dr. Andrew Feinberg, Gilman Scholar and director of the Center for Epigenetics in the Institute for Basic Biomedical Sciences at the Johns Hopkins University School of Medicine, added: “It’s likely that when food supplies are highly variable, these epigenetic changes help our bodies adapt to temporary surges in calories. But if the high-calorie diet continues over the long term, the same epigenetic pattern raises the risk for disease.”
Evidence from the study indicates the epigenetic changes linked to obesity affect genes that can raise the risk of diabetes. The researchers now hope these results could see an epigenetic test developed which can detect diabetes much earlier.
“In further tests, we showed that at least some of these genes indeed regulate insulin action on sugar uptake; they offer insights into new potential targets for treating type 2 diabetes,” Wong concluded.