You know that fried chicken is sinful, but why can't you let it go? | Nature sub-journal

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We obviously know that Coca-Cola fried chicken is very sinful , but why can’t we control ourselves...

Is this a distortion of human nature or a loss of self-control?

A team of neuroscience researchers in the United States studied this issue.

They discovered some special neurons in a certain part of the brain. This group of clever little ghosts can help you start a "hedonic eating" state, allowing you to eat fried chicken, fried skewers, cola, milk tea and other high-sugar and high-calorie foods. The more I eat, the more I want to eat.

On the contrary, if these neurons are inhibited, it will not only reduce the brain's desire for high-calorie and high-sugar foods -

even! Even the willingness to exercise is stronger!

This latest result has been published in Nature Neuroscience, a Nature subsidiary journal.

How is it proven? Look down.

The switch of the "eating and pleasure" mode in the brain

The researchers chose mice as their experimental subjects. Like humans, they are groveling slaves in front of high-calorie and high-sugar foods .

These experimental mice are all over 2 months old, and are kept in cages in groups of 2-5. The lighting time and temperature are set according to the appropriate environment for the organism, and the experiment has been approved by the relevant animal protection and use agencies.

Researchers believe that our interest in high-sugar and high-fat foods stems from the fact that the interstitial nucleus of the anterior commissural hindlimb (IPAC) in the brain is activated by taste stimulation, activating the "meal hedonic" mode.

Since there is no research on IPAC's energy homeostasis, they started an experiment .

The researchers first tested how the diet activated specific areas of the brain.

In the figure below, the number of green dots represents the degree of neuron activation. The left side shows the activation of various parts of the brain when eating is restricted, and the right side shows the status of eating for 30 minutes.

The results showed that after eating, the IPAC and basal striatum (FS) areas in the brain were significantly activated:

Furthermore, the researchers changed the feeding food to high-fat lard. Comparing the two pictures above, the green part of the IPAC increased significantly, while other brain parts such as the basal striatum (FS) did not change significantly.

This illustrates that IPAC is related to high-fat foods.

The researchers looked specifically at the extent to which different foods produced feelings of happiness.

It was found that feeding high-fat foods provided the strongest pleasure to the brain, followed by grains. But compared with cereals, the pleasure value of high-fat foods is nearly twice as high.

Then compare the pleasure produced by different liquid foods .

The mice were fed different contents of sugar and fat fluids respectively. Not surprisingly, the pleasure produced by high sugar or high fat was much higher than that of restricted eating, and the pleasure of 5% high-fat liquid food was much higher than that of 0.5% low-fat liquid food. .

The researchers believe that the IPAC part is more like a hedonic eating than purely for survival.

Considering that the sense of smell is also a major factor in arousing appetite , the research team designed a separate device to release the aroma of oil, food spoilage (BA) and mineral oil (MO) to observe the mice's reactions.

They found that the aroma produced by fat aroused strong pleasure in mice. Specifically, the IPAC part of the brain was significantly activated. However, in contrast, this part showed "insensitivity" to the smell of putrefaction and mineral oil:

On the basis of the above, the researchers conducted a reverse experiment .

They retested the mice's response to a grain-fed diet and a high-fat diet by injecting a specific chemical (KORD) that inhibits the IPAC portion.

The results showed that mice with IPAC inhibition had reduced intake of both grain-fed and high-fat foods, but not water intake. In addition, their energy expenditure and exercise volume also increased .

Furthermore, they inactivated IPAC for a long time and found that the homeostatic feeding behavior of mice (TeLC group) was impaired, but the drinking behavior was not affected:

Regarding follow-up research, the research team revealed that they will explore the response of this part of neurons to different foods in more detail to find better ways to treat obesity.

team introduction

Finally, get to know the team members.

The first author is Alessandro Furlan, from Cold Spring Harbor Laboratory. His research field is neuroscience. He graduated with a PhD from Karolinska Institute in Stockholm.

The second author is Alberto Corona, now a postdoctoral fellow at the Icahn School of Medicine at Mount Sinai. This article is the result of research at Cold Spring Harbor Laboratory.

The instructor behind this article is Li Bo. Public information shows that this scientist graduated from Jining Medical College with a bachelor's degree, then obtained a master's degree from the Chinese Academy of Sciences, and a doctorate from the University of British Columbia in Canada. He is currently working at the Cold Spring Harbor Laboratory.

Reference links:
[1]https://doi.org/10.1038/s41593-022-01178-3
[2]https://www.eurekalert.org/news-releases/968561
[3]https://mp. weixin.qq.com/s/hH0RBjM7IIJIQJE82t-P3w
[4]https://facultyprofiles.cshl.edu/bo.li