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Updated 09 December 2019

Your stretching intestine - not stomach - is what tells your brain you're full

New research suggests it’s your engorged intestine that tells your brain to switch off your appetite when you've had enough to eat.

After gorging yourself on stacks of pancakes, you start feeling unpleasantly full, but how does your body actually know when you've had enough?

The sensation of a full stomach has long been believed to be what tells us to stop eating, but new laboratory research led by UC San Francisco neuroscientist Zachary Knight suggests that a stretched intestine may play an even bigger role in making us feel sated.

As food moves from your mouth down your oesophagus, it eventually lands in your stomach and fills the space. This leads to the stretching of the muscular wall, which slowly expands like a balloon.

There’s a multitude of nerves wrapped around the stomach wall, and when these nerves sense the stretching, they communicate with an extensive web of gut nerve endings, collectively called the vagus nerve, up to the brainstem and hypothalamus – the main parts of the brain that control food intake. 

For a long time, scientists believed that this nerve feedback is what is responsible for the brain sensing when we’re full, but until now there wasn’t much clarity on the roles of the various nerve cells (or neurons) in the gut.

"Given how central eating is to our lives, it is remarkable that we still don't understand how our bodies know to stop being hungry when we eat food," said Knight.

The study

To figure out this puzzle, the Knight lab team, led by postdoctoral researcher Ling Bai, a neuroscientist at the University of California, San Francisco, started by using genetic sequencing to create a map of the different neurons in the GI tract.

They then genetically engineered the neurons of mice to be activated by light. This allowed them to easily stimulate those specific neurons and see which affected the rodents’ appetites.

The researchers activated the neurons that detect stomach stretch, and found that the unfed mice ate less because they felt like their stomachs were already full, which was something scientists already knew. What they didn’t know, however, was that mice would barely have an appetite when the neurons that detect stretch in the intestines were activated. And when those neurons stopped being stimulated, the mice returned to eating normally.

"This was quite unexpected, because the dogma in the field for decades has been that stomach stretch receptors sense the volume of food being eaten and the intestinal hormone receptors sense its energy content," Bai said.

What do these results mean?

The findings from the research could provide insight into how stretch receptors can be manipulated to treat medical conditions related to nutrition, such as obesity.

More than this, it suggests a potential explanation for why bariatric surgery is effective at promoting long-term appetite and weight reduction, notes the research report, and could answer the mystery of the mechanism known to effectively block hunger after surgery.

"Identifying the mechanism by which bariatric surgery causes weight loss is one of the biggest unsolved problems in the study of metabolic disease, and so it is exciting that our work could suggest a fundamentally new mechanism for this procedure," Knight said. "At present, however, this idea is a hypothesis that still needs to be tested."

Image credit: Getty

 
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