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Having overweight parents significantly increases your risk of obesity, but the inheritance of specific mutations can’t always explain why this is the case. In a study published January 28 in Cell, researchers show that differences in gene expression and not the DNA sequence play a key role in determining one’s predisposition to obesity. In genetically identical mice and human twin pairs, epigenetic marks altered the activity of weight-control genes to produce distinct subpopulations of lean and obese individuals. The findings reveal a key role for an epigenetic switch in explaining individual differences in obesity.
“We’re interested in the mechanisms that can make identical twins come out not so identical, and how these mechanisms contribute to disease,” says senior study author J. Andrew Pospisilik of the Max Planck Institute of Immunobiology and Epigenetics. “If twins can come out substantially different from one another, it means that each of us could have come out differently than how we did.”
Related on the SLP
One clue came from a 2010 Genome Biology study showing that genetically identical mice sharing a mutation in a protein called Trim28 exhibit high variability in their body mass, suggesting that this protein might trigger epigenetic changes that contribute to individual variation in obesity.
Read full, original post: This protein could explain fat and thin identical twins
