Follow Up: The Obesity Gene

Despite years of extensive research, there is still much we do not understand about obesity. As a follow up to our blog post “Obesity Gene May Hold the Key to Eradicating Obesity,” we’ve been following the research of scientists in Germany that say they’ve discovered a genetic ‘switch’ that could essentially turn obesity on or off.

The new study is founded on epigenetics research, the way the genes in our body change based on chemical and environmental factors. According to this line of thought, we are born with a set of genes that can be turned off or on, dialed up or down through processes inside the body. This usually explains why identical twins don’t always look identical.

The scientists in Germany have discovered one of these epigenetic tags, which apparently works like a light switch. “Once the switch is triggered, it is a lifelong decision that ends in a stable, either lean or obese phenotype,” said lead author Andrew Pospisilik from the Max Planck Institute of Immunobiology and Epigenetics.

According the researchers, the effect is similar to an ordinary light switch – on or off, lean or obese. Typically, we consider epigenetic control of disease to act more like a dimmer, shifting phenotypes gradually up or down.

Previous studies have shown a link between Tim28 and the genes that control weight so researchers hypothesis that this is an epigenetic tag that can control obesity in a binary way.

While we know that epigenetic information can be passed through the generations in animals, there are still a lot of unanswered questions. The biggest question remains, how might this work in humans?

This new study might help us understand how genetic variations are passed on, as well as leading the way towards improved treatments for those living with obesity. The next step is to determine whether factors such as diet, stress or drugs can also flip the switch on or off.

Source: ScienceAlert 

Last updated on February 29, 2016, posted in: News, Recent research by
Comments are closed.