Goodbye Obesity, Hello Weight Loss? Scientists Find 'Stop Eating' Switch In The Brain (Of A Mouse)
18 March 2016, 10:52 am EDT By Katherine Derla Tech Times
Researchers found the "Stop Eating" switch in the brains of mice that can signal when to stop eating. When confirmed, the research can lead to novel intervention methods to help fight obesity and assist in weight loss and maintenance. ( Thomas Rydberg | Flickr )
Scientists found - by accident - a nerve cell type that seems to control a mouse's feeding behavior and tells it to stop eating. In other words, they found a "Stop Eating" switch in the animal's brain and, when confirmed, could lead to novel ways in obesity treatments in humans.
Researchers from the Johns Hopkins University School of Medicine believed that the bloodstream's sugar levels play a role in turning on this "switch" during meal times. If the switch is turned on, it can make people feel full so they will stop eating. However, if the switch is turned off or fails, it often results in overeating, which leads to obesity.
"When the type of brain cell we discovered fires and sends off signals, our laboratory mice stop eating soon after. The signals seem to tell the mice they've had enough," said Richard Huganir, Department of Neuroscience director at the Johns Hopkins University School of Medicine.
In the study published in the Science journal on March 18, the researchers initially studied the strength of connections between the brain's nerve cells, which is vital in memory and learning.
In the mice study, they experimented by turning off a gene for the OGT enzyme in particular regions of the brain. The OGT enzyme plays many roles in body metabolism such as the usage of glucose and insulin.
One of the OGT enzyme's jobs is the addition of a glucose chemical derivative - a molecule called N-acetylglucosamine (GlcNAc) - to proteins. When the gene that codes for OGT is deliberately removed or knocked out in a particular nerve cell type in the hypothalamus, the mice's weight doubled in three weeks because of fat buildup.
The mice that didn't have OGT ate the same number of meals, but failed to know when they're already full. They continued to eat and doubled their weight compared with mice with a functioning OGT.
"This gene for the OGT enzyme regulates the balance of the satiety effect. When we artificially increase the activity of the gene, for instance, we can stop a normal mouse that is hungry from eating," added Huganir.
They found that the "Stop Eating" or appetite switch might be controlled by the levels of glucose sugar in the bloodstream. Glucose sugar levels rise naturally after a meal or after ingesting sugary drinks. The researchers believe that glucose and OGT work together in portion size control.
Photo: Thomas Rydberg | Flickr
Scientists found - by accident - a nerve cell type that seems to control a mouse's feeding behavior and tells it to stop eating. In other words, they found a "Stop Eating" switch in the animal's brain and, when confirmed, could lead to novel ways in obesity treatments in humans.
Researchers from the Johns Hopkins University School of Medicine believed that the bloodstream's sugar levels play a role in turning on this "switch" during meal times. If the switch is turned on, it can make people feel full so they will stop eating. However, if the switch is turned off or fails, it often results in overeating, which leads to obesity.
"When the type of brain cell we discovered fires and sends off signals, our laboratory mice stop eating soon after. The signals seem to tell the mice they've had enough," said Richard Huganir, Department of Neuroscience director at the Johns Hopkins University School of Medicine.
In the study published in the Science journal on March 18, the researchers initially studied the strength of connections between the brain's nerve cells, which is vital in memory and learning.
In the mice study, they experimented by turning off a gene for the OGT enzyme in particular regions of the brain. The OGT enzyme plays many roles in body metabolism such as the usage of glucose and insulin.
One of the OGT enzyme's jobs is the addition of a glucose chemical derivative - a molecule called N-acetylglucosamine (GlcNAc) - to proteins. When the gene that codes for OGT is deliberately removed or knocked out in a particular nerve cell type in the hypothalamus, the mice's weight doubled in three weeks because of fat buildup.
The mice that didn't have OGT ate the same number of meals, but failed to know when they're already full. They continued to eat and doubled their weight compared with mice with a functioning OGT.
"This gene for the OGT enzyme regulates the balance of the satiety effect. When we artificially increase the activity of the gene, for instance, we can stop a normal mouse that is hungry from eating," added Huganir.
They found that the "Stop Eating" or appetite switch might be controlled by the levels of glucose sugar in the bloodstream. Glucose sugar levels rise naturally after a meal or after ingesting sugary drinks. The researchers believe that glucose and OGT work together in portion size control.
Photo: Thomas Rydberg | Flickr
