The study found a ‘switch-like mechanism’ that causes some individuals with identical genetic material - such as twins - to be lean or obese.
Much like a light-switch there are only two outcomes - on and off.
The team had previously observed that large numbers of twin mice displayed significant variations in bodyweight, despite being genetically identical.
The researchers were therefore keen to explore the mechanisms that make identical twins come out not so identical, and how these mechanisms contribute to disease.
Senior author J. Andrew Pospisilik, a researcher at the Max Planck Institute of Immunobiology and Epigenetics said: “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."
More specifically, the researchers wanted to figure out if the genes associated with obesity risk could be altered.
They did this by testing twin mice with the same obesity gene (Trim28) mutation. When Trim28 mutates it can either trigger an obese or lean outcome.
They did this by testing twin mice with the same obesity gene (Trim28) mutation. When Trim28 mutates it can either trigger an obese or lean outcome.The team were able to turn genes on and off in a process called ‘polyphenism’ in order to see which would affect obesity.
The mice deficient in Trim-28 had strikingly different body masses to their twin with the Trim28 gene.
A Trim-28 deficiency impacted other genes that altered growth and body weight.
To further their study, the researchers looked at fat tissue from 22 lean and 18 obese children and the results were intriguing.