THE EPIGENOME has been revealed to play a significant role in diabetes onset, providing clues into how genes and the environment interact to proliferate this worldwide phenomenon.
To investigate the potential role of epigenetics in Type 2 diabetes (T2D) incidence, Dr Andrew Feinberg, Gilman Scholar and Director of the Center for Epigenetics, Institute for Basic Biomedical Sciences, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA and colleagues collaborated with the group led by Dr G. William Wong, Associate Professor of Physiology, Center for Metabolism and Obesity Research, Johns Hopkins University School of Medicine to test the epigenetics of identical mice by feeding them either normal or high-calorie diets.
Epigenetic chemical tags influence whether and how often genes are activated, without affecting the genetic code itself; Dr Feinberg likened the behaviour of the epigenome to “software” running the DNA’s “hardware”. Epigenetic marks at over 7 million sites in the DNA of the mice’s fat cells were analysed, and there were significant differences between the normal and obese mice. It was observed that some sites with chemical tags called methyl groups were present in lean mice but absent in their obese counterparts and vice versa. This pattern was also observed in humans in a separate study.
“Mice and humans are separated by 50 million years of evolution, so it is interesting that obesity causes similar epigenetic changes to similar genes in both species,” said Dr Feinberg. “It is 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.”
Dr Feinberg added that the results could pave the way for an epigenetic test which could identify individuals at risk of developing diabetes in the future.