This activates the gut-brain connection the desire to eat more fat

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Surely it happens to you, when you eat fats you have a greater impulse to continue eating them. The culprit behind this irrepressible desire could be hiding in a mechanism that connects the intestine with the brain, activated by the intake of lipids.

Normally, when foods with fat are consumed, the desire to continue consuming them in subsequent days increases, something that increases the risk of obesity, the great health problem of this century. There has always been a doubt as to why this impulse to eat fats appeared, it was thought that it could be due to the specific taste of these foods, which tempted us to gobble up more than we should, however, a study from Columbia University ( USA) has shown that this fatty craving is due to a new connection between the gut and the brain.

Specifically, the work has revealed that, after being ingested, the fat activates sensors in the intestines that send a signal, conducted along the nerves to the brain, stimulating it and generating that desire to eat fat again.

Sugar and fat are two of the common components in ultra-processed foods, a type of product that is consumed in excess and that creates a certain addiction. Already in previous studies it was found that sugar triggered a series of brain signals after ingestion, the new work, published in the journal Nature, seems to describe a similar operation with fats.

Neurons of the vagus nerve send signals to the brain when taking fats

The origin of our desire to eat fatty foods is in the intestine, to prove it, the researchers took a group of mice that were offered bottles of water, some with dissolved fat, and others with sweet substances based on artificial sweeteners that they tasted appealing but had no effect on the gut.

The results showed that the mice found both drinks attractive at first, but 48 hours later they showed a greater preference for those with dissolved fats. That preference held true even when scientists genetically modified the mice to remove their ability to taste fat with their tongues. “Although the animals could not taste the fat, they were driven to consume it,” said the author of this work.

“The tongue tells our brain what we like, however, the intestine tells our brain what we want, what we need”

This, according to the researchers, would happen because sweeteners send signals to the brain when they come into contact with the tongue, but once they are swallowed they have no greater effect. In the case of fats, this is not the case, but these lipids continue to send signals to the brain of their presence even when they reach the intestine, which increases the desire to consume it.

Put it more graphically by Dr. Zuker, Charles Zuker, professor of biochemistry and molecular biophysics and neuroscience at Vagelos College of Columbia and lead author of the study, supported by the Howard Hughes Medical Institute: “Our research shows that the tongue tells our brain what we like, like things that taste sweet, salty or greasy, however, the intestine tells our brain what we want, what we need”.

So, they began to look for where that specific brain circuit capable of activating that response of the mice’s desire for fat was activated. And boy did they find it. They discovered that the area of ​​the brain that is activated when we eat fat is the caudal nucleus of the solitary tract (cNST) in the cervical trunk. In addition, they found that specific neurons in the vagus nerve send stimuli to the brain caused by ingested fat. An important finding that could be useful to create drugs that block these signaling pathways, thus reducing the desire to consume lipids.

Researchers have discovered the area of ​​the brain that is activated by eating fat, so now it remains to find drugs to block these signals

And it is that, the next step taken by another main author of this project, Dr. Mengtong Li, was to block the activity of these cells by means of a drug. Shutting down signaling from either group of cells prevented the vagal neurons from responding to fat in the intestines. He then used genetic techniques to turn off the vagal neurons themselves or the neurons in the cNST. In both cases, the mouse lost its appetite for fat.

“There are two types of people who can benefit from these interventions. One is that of people who have a clinical problem. In that case, you could intervene with some compound that allows you to begin to dissociate these two circuits. The second is looking at the general consumer”, explains Zuker.

“There the logic would work as in artificial sweeteners, but with the difference that not only the tongue is satisfied, but also that intestine-brain circuit. Conceptually, perhaps there is a way in which we can maintain the attraction to sugar or fat, but without having the calories, “concludes the expert.

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