Switching Off Obesity Genes Possible to Stay Lean: Study

For those who are struggling with their weight, a new study published in Cell journal suggests that there is a switch like mechanism that determines when one can be lean or obese.

The researchers discovered the reason why obesity genes are triggered in some children born to overweight parents, but not to others, Medical Daily reported.

"We're interested in the mechanisms that can make identical twins come out not so identical, and how these mechanisms contribute to disease," said senior study author J. Andrew Pospisilik, a researcher at the Max Planck Institute of Immunobiology and Epigenetics, in a press release. "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."

To determine if the obesity genes can be altered, the team tested twin mice with the same obesity gene mutation. They learned that, when the obesity gene, Trim28 mutates it triggers genes to produce either lean or obese individuals. Since the subjects of the study were twins and have the same genetic backgrounds, they were able to turn genes on and off to see which ones would gain weight. The concept is called polyphenism.

Pospisilik and his team produced a large population of twin mice. One group has Trim28 and the other has none. The mice have identical genes and were raised as equally as possible. The researchers found out that those without Trim28 have different body masses.

Trim28 deficiency affected other genes; it turned on Nnat and Peg3. Both genes alter the growth and body weight.

"A switch-like mechanism to produce individuals with different traits without changing DNA provides a selective advantage at the population level," Pospisilik said. "Polyphenism allows an emergency or plan B version that gets the species through transient selective pressures."

Per Express, to further the study, the team examined the fat tissue from 22 lean and 18 obese children. They found out that just as the result of the mice study, children with Trim28 deficiency were obese. The also examined the published data from identical twins and the same trend was present, which supported the results of their study.

"Our data not only helps to understand the interaction of genetic and epigenetic factors in obesity and other diseases, they have implications for how we think about evolution," Pospisilik said.

"Our next major goal is to see whether we can modify this process whether we can turn the disease switch on or off by supplementing diet, minimizing stress, or giving epigenetically relevant pro-drugs. The hope is that we can permanently flip the system back to lean in one shot."