Stay up to date with notifications from The Independent

Notifications can be managed in browser preferences.

‘Hunger-controlling’ cells discovered in the brain may lead to new way to treat obesity

Treating people for being overweight or obese costs the NHS more than £6bn a year

Fiona Keating
Tuesday 01 August 2017 05:33 EDT
Comments
Certain neurons in the brain have a function in feeding behaviour
Certain neurons in the brain have a function in feeding behaviour (Reuters)

Your support helps us to tell the story

From reproductive rights to climate change to Big Tech, The Independent is on the ground when the story is developing. Whether it's investigating the financials of Elon Musk's pro-Trump PAC or producing our latest documentary, 'The A Word', which shines a light on the American women fighting for reproductive rights, we know how important it is to parse out the facts from the messaging.

At such a critical moment in US history, we need reporters on the ground. Your donation allows us to keep sending journalists to speak to both sides of the story.

The Independent is trusted by Americans across the entire political spectrum. And unlike many other quality news outlets, we choose not to lock Americans out of our reporting and analysis with paywalls. We believe quality journalism should be available to everyone, paid for by those who can afford it.

Your support makes all the difference.

Cells in the brain that may help control the hunger impulse have been discovered in a development that could lead to new treatments for obesity.

The research adds weight to the evidence that eating is a surprisingly complex biological behaviour.

“We have identified two new populations of cells in the brain that potently regulate appetite,” said Alexander Nectow, who published a paper about the study in the journal Cell.

The area of the brainstem under scrutiny is the dorsal raphe nucleus (DRN), where the two types of cells are located.

It is thought new drugs to treat obesity by controlling hunger messages that prompt people to seek out and consume of food could be targeted at those cells.

Dr Nectow, an associate research scholar at Princeton University, found that the DRN section of the brain becomes activated in hungry mice. This was discovered when images were taken using a pioneering technique called iDisco.

Imaging other mice that were given more than their normal amount of food showed a different pattern of DRN activity. This showed that neurons in this part of the brain clearly had a function in feeding behaviour.

Further research is needed to ascertain which types of neurons that make up the DRN are involved in the process.

“There are two possibilities when you see something like that,” Dr Nectow said.

“One is that the cells are just along for the ride – they are getting activated by hunger but they’re not actually driving the food intake process.

"The other possibility is that they are in fact part of the sense-and-respond mechanism to hunger – and in this case, we suspect the latter.”

Pioneering research into obesity in the 1990s led to the discovery of the effect of leptin on appetite. It is a hormone which acts on neurons in the hypothalamus area of the brain which suppresses appetite.

An injection of the hormone led to dramatic weight loss in patients with leptin deficiency, but it was also found that there was no effect on many obese people.

"Obesity is generally associated with leptin resistance," said Dr Friedman, whose lab produced the study. "And our recent data suggest that modulation of the activity of specific neurons with drugs could bypass leptin resistance and provide a new means for reducing body weight."

The new research findings could be effective in creating treatments for obesity and its related issues including diabetes. According to Public Health England, treating overweight and obese people costs the NHS more than £6bn a year.

One-fifth of the world’s adults are expected to be obese by 2025, according to a paper published in The Lancet.

Join our commenting forum

Join thought-provoking conversations, follow other Independent readers and see their replies

Comments

Thank you for registering

Please refresh the page or navigate to another page on the site to be automatically logged inPlease refresh your browser to be logged in