Obesity treatment hope
Researchers used mice to identify which neurons controlled hunger
A STUDY identifying which neurons in the brain control hunger could aid in the development of drugs to tackle obesity, researchers have said.
Researchers, including a scientist from Edinburgh University, activated a specific brain circuit in mice to make the animals feel full and prevent them f rom over-eating.
Their discovery shows that this brain circuit not only promotes full- ness in hungry mice but also removes the almost painful sensation of grating hunger, findings that could provide a promising new target for the development of weight-loss drugs.
The findings, published in the journal Nature Neuroscience, identify the long-sought neural link that inhibits and controls eating – a melanoncortin 4 receptor-regulated (MC4R) circuit in the brain.
In order to gain direct access to these MC4R neurons, the authors used a group of mice genetically engineered to release a protein in these particular brain cells.
This enabled the scientists to map their connections and remotely control their activity.
The US team was led by Dr Alastair Garfield, a visiting professor and physiologist from Edinburgh University.
He said: “Although these mice had eaten a day’s worth of calories and were fully sated, when we used (a laboratory technique) to turn off these brain cells they began to ravenously consume food for which they had no caloric need.”
He adds that the opposite also held true: artificially activating these satiety neurons prevented unfed hungry mice from eating.
“Together these experiments suggested that (these) neurons function like a brake on feeding and are essential to prevent overeating,” said Dr Garfield.
Scientists at the Lowell labora- tory, a department of Harvard Medical School where the study was conducted, have spent the last two decades creating a wiring diagram of the complex neurocircuitry that underscores hunger, feeding and appetite.
Their group, along with others, made the key discovery that Agouti-peptide-expressing (AgRP) neurons, a small group of neurons located in the brain’s hypothalamus, detect caloric deficiency and drive intense feeding.
The latest study moves the research on a level, however, by identifying the neurons “downstream” of the AgRP neurons which were actually causing the activation and inhibition of hunger.
Dr Bradford Lowell, the study’s co-senior author and Professor of Medicine at Harvard Medical School, said: “Determining the identity of these ‘satiety’ neurons is the key to establishing the blueprint for how the brain can regulate appetite.
“It was an important missing point of connection in the wiring diagram.”
A key component of the study was a behavioural experiment.
This was designed to clarify whether the mice ate to get rid of an unpleasant feeling of hunger or because they found eating rewarding.