High-Fat Diet Weakens 'Stop Eating' Signals in Mice

In a breakthrough study that could help tackle the global obesity epidemic, a team of researchers has discovered that high-fat diets can result in a loss of 'brake' signals used to control appetite. In experiments conducted on mice, the team found that certain foods can influence the body's drive to eat and stop glutamatergic nerve cells from sending "full" signals to the brain.

Fatty diets trigger obesity in mice

The findings were published in the journal Science and explain how mice that were fed high-fat chow for just two weeks experienced a slump in the activity of brain cells responsible for sending "stop eating" signals to the brain. For the team, the results offer new insight into the underlying relationship between eating habits and appetite. The study also reinforces the dangers of overeating and serves as a reminder that while natural appetite cues are critical to survival, when thrown off balance they can have a serious impact on health.

Garret Stuber, a neuroscientist at the University of Washington in Seattle explains how the brain is equipped with a multitude of appetite systems designed to ensure the body receives enough food and energy. These systems are in an area of the brain known as the lateral hypothalamus, which is directly involved in eating behaviours. It's made up of a large number of diverse cells, including a group known as glutamatergic nerves. When investigating the impact of a high-fat diet Stuber and his team found that cellular glutamatergic nerve activity in obese mice was significantly slower than in their lean counterparts.

A slump in glutamatergic cell activity  

The study built on previous research suggesting that glutamatergic cells act as a 'brake' to curb the appetite and send "fullness" signals to the brain. The new research published in Science confirms that high fat diets block glutamatergic nerve cells and stop them from firing signals, which spurs an increase in appetite and triggers a gradual shift towards obesity.

“Obesity doesn’t just happen overnight,” explains Stuber. Instead, he asserts it can be a slow transition aided by sluggish glutamatergic cells activity as a result of a high-fat diet. For neuroscientist Stephanie Borgland, the results suggest that “these cells’ decreased activity is removing the brake on feeding and obesity.”

The role of the hypothalamus

While it's unclear if a high fat diet in humans triggers the same blockage of appetite-suppressing nerve cells, brain-imaging studies suggest that the hypothalamus, the same region of the brain associated with eating behaviours in mice, is also involved in signalling hunger and fullness.

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