Scientists find 'switch' in the brain that helps control appetite

Scientists have found a “switch” in the brain that helps to control appetite, which could explain why some people find it hard to know when to stop eating, a study has suggested.

The researchers believe that sugar levels in the bloodstream are involved in triggering when the switch is turned on during a meal so that people begin to feel full. But when the switch fails, it leads to overeating and obesity, they suggested.

The findings, which could provide further scientific evidence to support George Osborne’s new sugar tax, are part of a wider body research into the nature of appetite control and how hormones and brain activity are both involved in determining hunger, craving and over-eating.

Scientists discovered the appetite switch while studying the strength of the connections between nerve cells in the brains of laboratory mice, a phenomenon known to be important for learning and memory.

In particular they wanted to see what would happen when the gene for an enzyme called OGT was deliberately knocked out in certain regions of the mouse brain.

OGT is known to be involved in many aspects of body metabolism, including the use of the hormone insulin and glucose in the bloodstream – which can rise during a meal or after drinking sugary drinks.

One of the jobs of the enzyme is to add a chemical derivative of glucose to proteins and this appears to be important certain nerve cells of the appetite control centres of the brain. When the gene for this enzyme is deleted or knocked out, the mice doubled in weight in just two weeks as a result of a build-up of fat.

“These mice don’t understand that they’ve had enough food, so they keep eating,” said Olof Lagerlof, a Johns Hopkins researcher and first author of the research published in the journal Science.

The scientists found that when the OGT gene no longer worked in a certain type of nerve cell in the hypothalamus of the brain, the mice did not seem to know when to stop eating and grew excessively fat compared to ordinary mice, said Professor Richard Huganir, director of the department of neuroscience at Johns Hopkins University School of Medicine in Baltimore, Maryland.

“Two weeks later we were going to study behaviour and learning but my graduate student, Olof, came back and told me that these mice were getting really fat, which we didn’t expect, so we started to study what was causing that,” Professor Huganir said.

“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,” he said.

“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,” he added.

However, when the nerve cells did not function in the “knock out” mice, the mice completely lost their send of appetite control.

“They ate the same number of times each day as ordinary mice, but they lingered over their food, eating for longer with the result that they ate twice as much as they would normally,” Professor Huganir explained.

The appetite switch is controlled by the amount of glucose sugar circulating in the bloodstream, which naturally rises after a meal – or after drinking a sugary drink.

“It’s very likely that the same mechanism and cell type in the brain are also found in humans. We think this type of appetite control mechanism probably occurs in humans, but we need to do more work to show that,” Professor Huganir said.

“In theory, if we really understand what’s occurring here we might be able to deliberately target this mechanism with drugs that could control appetite, which could help in the fight against the obesity epidemic,” he said.

The researchers believe the study could form part of a new approach to controlling obesity where drugs or treatments are targeted at specific pathways in the brain that can control appetite more effectively than through voluntary control and dieting.