Scientists discover way brain wreaks havoc on our dieting
- Researchers used a tiny periscope to access part of brain not accessed before
- Allowed them to gain deeper understanding of how we react to food cues
- Certain hunger-promoting neurons can be artificially turned on even when full
- Hopes that these same neurons can be turned off to reduce food cravings
- Could help obese people with a’faulty’ hard wiring that causes overeating
- ‘It’s a major advance to learn that we can artificially turn them on,’ says expert
Claudia Tanner For Mailonline
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A new drug that ‘switches off’ our food cravings could be possible after a breakthrough in understanding the way our brains govern hunger.
Scientists have identified the mechanism by which we feel hunger and then choose whether or not to reach for the biscuit jar.
Researchers made the discovery thanks to a pioneering new use of a tiny periscope which allowed them to see neurons in a previously unobservable part of the brain.
Their findings could help people with ‘faulty’ hard wiring in their brain that does not allow them to stop eating when full.
‘To put it simply, when you’re hungry, the picture of a cheeseburger may be extremely appealing and effective in influencing your behavior,’ explained lead author Yoav Livneh, postdoctoral fellow at Beth Israel Deaconess Medical Center at Harvard University.
Scientists think they can switch off neurons in the brain causing us to seek our more food (file)
‘But if your belly is full after eating a big meal, the same cheeseburger picture will be unappealing.
‘We think that the pathway we discovered from hunger-promoting neurons to a region of the brain called the insular cortex plays an important role here.’
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ANTI-OBESITY JAB THAT INJECTS VIRUS COULD BE IN PIPELINE
Scientists said they have discovered a way to influence appetite, which they hope can eventually be used to treat obesity.
Researchers in London were able to successfully alter the way mice ate with a virus that targeted just thyroid receptors in the brain.
This previously has been difficult because thyroid hormones also help to control the nervous system, body temperature and cholesterol levels.
Researchers are hopeful their work can lead to an anti-obesity drug because the study was successfully able to only affect the mice’s appetite.
The experiment was conducted by the Imperial College London and used a virus to deactivate thyroid hormone receptors in the part of the brain that controls appetite.
Mice given a shot that contained the virus ate more food, doubling in size to 40 grams over the course of six weeks.
Rodents that were not given the virus remained stable at a weight of 20 grams.
Experts concluded that the virus was able to successfully target the hypothalamus, which controls appetite, without causing additional side effects in the treated mice.
Obese people’s over-sensitivity to food cues
Brain imaging data supports the idea that the insular cortex – part of the brain – is involved in deciding if a source of food is worth pursuing.
In people of a healthy weight, the insular cortex increases its activity in response to food cues – the sight of a cheese burger for instance – during hunger but not following a meal.
Studies suggest that this process often goes awry in people with obesity or other eating disorders that involve excessive cravings.
Those findings indicate that specific changes in brain activity, including increased sensitivity to food cues, may underlie these disorders – rather than a ‘lack of willpower’.
And so the researchers wanted to find out more about how this happens, tetsing on ,mice which are biologically very similar to humans.
They used a periscope to monitor and track individual neurons in awake mice as they responded to food cues in both sated and hungry physiological states.
Key findings
Their experiments showed that when they were presented with food, a certain group of neurons in the insular cortex were activated, which were responsible for mice choosing whether or not to eat.
After they had eaten until they were full, this brain response to food cues in the insular cortex was no longer present.
While the mice were still full, the researchers used genetic techniques to artificially trigger them wanting more food by ‘turning on’ specific neurons in the hypothalamus, a part of the brain that has a vital role the regulation and control of hunger.
By activating these neurons, called AgRP, the team caused mice that were full to once again react to cues and seek more food.
As a result, the hope therapies could dial down this neuron behaviour and reduce excessive cravings.
‘These AgRP neurons cause hunger – they are the quintessential hunger neuron,’ explained co-author Bradford Lowell.
‘It’s a major advance to learn that we can artificially turn them on and cause full mice to work to get food and to eat as if they hadn’t eaten in a long time.
‘We’re still trying to understand how this process works.
‘Huge questions remain, but they are now addressable thanks to these new imaging methods.’
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