Scientists have announced that they have found the trigger and potentially the “cure” for obesity.
According to a study published in the Science journal – obesity can be easily controlled by clicking a switch in the brain.
An enzyme found in the brains of mice and humans, O-GlcNAc transferase (OGT) appears to control our ability to determine whether or not we feel full.
Researchers removed this enzyme from one group of mice in a study – and found that the mice ended up eating twice their normal amount of food, becoming much fatter in the process.
When the amount of food available to the mice was restricted to a normal dose, their weight remained the same. This finding suggests that the enzyme determines food cravings. When the scientists increased the level of the enzyme in another group of mice, they ate much less food and became leaner in the process.
The enzyme is O-GlcNAc transferase, or OGT, which is known to work in a chemical pathway controlled by nutrients and metabolic hormones, particularly insulin. That pathway has long been linked with obesity. But researchers knew almost nothing about how the pathway linked to the metabolic disorder or OGT’s specific role.
To figure it out, researchers tried the simple genetic approach of deleting the enzyme from mice and looking to see what, if anything, changed. The researchers, led by Richard Huganir at Johns Hopkins University School of Medicine, used a virus-based genetic tool to take out the enzyme from the noggins of adult mice and quickly noted a shift in the altered rodents’ eating habits.
With the freedom to eat however much they wanted, the modified mice gulped down more than double what their non-genetically engineered counterparts had at each meal—though both groups ate about the same number of meals. Within three weeks, the OGT-deletion mice became fat, tripling their body fat with no gain in lean mass. But if the modified mice were only allowed to eat a normal amount of food, they stayed a healthy weight.
In a closer comparison of the modified and normal mice, the researchers noted that the loss of OGT was linked to changes in a specific region of the mousey brain: the hypothalamic paraventricular nucleus (PVN), which is known to be involved in regulating appetite. In normal mice, OGT-filled nerve cells in the PVN light up after eating a big meal, the researchers found. In the OGT-deletion mice, these nerve cells stayed quiet.
Using a light-based genetic trick, the researchers reactivated the quieted nerve cells, trying to reverse the effect of deleting OGT—and they did. With the PVN nerve cells fired up, the fat OGT-deletion mice independently cut down on their food intake within 24 hours.
Overall, the data suggests that the OGT enzyme is a critical switch in a feedback loop that senses food signals, such as metabolic hormones, then fires up nerve cells to shut off the desire to eat. Without a properly working switch, mice ate more or less than normal.
Because the OGT pathway has already been linked to obesity in humans, the researchers are hopeful that the data could lead to a way to modify—or correct—satiation signals in people to treat obesity.
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