A Johns Hopkins research team has identified a type of brain cell that it is responsible for appetite control in rodents. The team found that if an enzyme is missing from the nerve cell the animals do not know anymore when to stop eating and, thus, they become obese.
Scientists report that mice without the enzyme OGT in their system became obese in about three weeks. If the findings are confirmed in human trials, they could pave the way to a revolutionary tool to prevent and cure obesity.
The findings were published Friday in Science.
Richard Huganir, lead author of the study, noted that whenever the brain cell was working properly it could signal mice that they ought to stop eating. The team discovered the brain cell responsible for appetite in mice during a study on synapse strength in the cortex and hippocampus.
In the latest study, Huganir and his team focused on OGT because the enzyme has been long known as an important catalyst in many biological processes such as insulin control and blood sugar metabolism. Plus, the enzyme shapes proteins’ behavior.
To find what role OGT plays in regulating appetite, researchers genetically altered laboratory mice’s brains not to release the enzyme anymore. Researchers observed that the rodents became obese in less than a month afterwards.
The team also learned that while rodents without the enzyme ate the same amount of meals per day, they ate more calories than their normal peers. Furthermore, when they were given the same amount of food as to the control group, the genetically modified mice stopped gaining weight.
Scientists concluded that the enzyme is responsible for appetite control, i.e. without it, the lab mice cannot sense when they had enough food.
Scientists, however, detected the new nerve cell in a brain area that regulates feeding, metabolism, and sleep: the hypothalamus. It was there that the OGT enzyme was missing from. The brain cell was detected in an area dubbed the paraventricular nucleus.
Scientists have long suspected that the paraventricular nucleus may be regulating food appetite. Brain scans showed that OGT-deficient brain cells had weaker synapses and three times as few brain cell connections as in normal cells.
Huganir concluded that the enzyme keeps synapses alive. Plus, he noted that in its absence there were so few synapses that the cells did not have enough input to beam the ‘stop eating’ signal.
Image Source: Wikimedia