Our culture has been obsessing over diets for at least a few decades, but despite all this time, there really hasn’t been any significant breakthrough. Sure, you can start a diet and you can either give it up or keep to it up to this day, but it doesn’t really guarantee that you’ll not fall into temptation.
So of course, people have been pining for years over a cheat code – something that will allow to lose weight without acquiring the necessary discipline. And despite the fact that that sounds kind of impossible, researchers from Johns Hopkins University School of Medicine found out that the brain contains an overeating off-switch.
O-GlcNAc transferase a.k.a. OGT
Known to function inside a chemical pathway generally controlled by metabolic hormones and nutrients, especially insulin, the OGT enzyme is relatively new discovery. Aside from the fact that the pathway has long been linked to obesity, the researchers didn’t really know much about the pathway or about OGT’s specific role.
After performing the study on mice abut which I’m going to talk in the next section, the team determined that OGT, O-GlcNAc transferase, is a very important switch in a sort of feedback loop that detects food signals, like metabolic hormones, and then it has some nerve cells shut off the desire to eat.
Since the OGT pathway had been linked to obesity before the study even started, the team is hopeful that they can use the data they found to somehow alter satiation signals in people. This way you wouldn’t have to abstain from anything, as you’d simply not feel the urge to consume it.
In order to test what the enzyme is capable of, the researchers of course tested it on mice. They used a genetic tool based on a virus to take out the enzyme from the brain of some rodents, while others were allowed to keep it, as a control group. The mice’s eating habits changed faster than in 24 hours.
The rodents that had the enzyme shut off ate more than twice the amount their non-affected siblings ate, tripling their body in just three weeks. However, when the change was reversed, the animals stopped overeating as fast as they started, and just as fast started reverting to a healthy weight.
Apparently, the loss of the OGT enzyme was linked to changes in the hypothalamic paraventricular nucleus, a specific region in the mouse brain known to regulate appetite. Normally, cells in the hypothalamic paraventricular nucleus light up after eating a big meal, but they stayed quiet for the OGT-less mice.
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