Overview: When fat enters the gut, a signal is generated that travels through neurons to the brain, driving cravings for fatty foods.
sauce: Columbia University
Dieters who struggle with greasy food cravings may be tempted to blame their tongues.The delicious flavors of butter and ice cream are hard to resist. A new study has revealed a whole new connection between the gut and brain that drives our cravings for fat.
At the Zuckerman Institute in Columbia, scientists studying mice have found that fat entering the gut triggers a signal. drive the desire for
Published September 7, 2022 Naturenew research raises the possibility of interfering with this gut-brain connection to prevent unhealthy choices and address the growing global health crisis caused by overeating.
“We live in an unprecedented time when excess fat and sugar intake is driving an epidemic of obesity and metabolic disorders,” says first author Charles Zuker of the Zuckerman Institute. Menton Lee, Ph.D., postdoctoral researcher at He completed his PhD with the support of the Howard Hughes Medical Institute.
“If you want to control your insatiable cravings for fat, science shows that the key pathway that drives these cravings is the connection between your gut and your brain.”
This new perspective on dietary choices and health began with the Zuker lab’s previous research on sugar. Researchers have found that glucose activates specific gut-brain circuits that communicate with the brain in the presence of intestinal sugar.
In contrast, zero-calorie artificial sweeteners do not have this effect, which may explain why diet soda does not satisfy us.
“Our research shows that the tongue tells our brain what we are doing. favoriteSweet, salty, fatty,” said Dr. Zukor, who is also a professor of biochemistry, molecular biophysics and neuroscience at the Bagueros College of Medicine and Surgery in Colombia.
“But the gut tells our brain what we’re doing. I want, what we need. “
Dr. Li wanted to see how mice responded to dietary fat. Lipids and fatty acids are what all animals must consume to provide the building blocks of life. She gave the mice a bottle of fat-dissolved water containing soybean oil components and water containing sweet substances known to have no effect on the intestines but to be initially attractive. gave me a bottle of
Rodents developed a strong preference for fatty water over several days. They formed this preference even when scientists genetically engineered mice to remove the animals’ ability to taste fat using their tongues.
“The animals couldn’t taste the fat, but they were nonetheless driven to consume it,” said Dr. Zuker.
The researchers reasoned that fat must activate specific brain circuits that drive behavioral responses to fat in animals. To look for that circuitry, Dr. Lee measured brain activity in mice while they were fed fat.
Neurons in the caudal nucleus of the solitary tract (cNST), a specific region of the brainstem, were activated. This was interesting because the cNST was also involved in the lab’s previous findings on the neural basis of sugar preference.
Later, Dr. Lee discovered a communication line that carried the message to the cNST. Neurons in the vagus nerve, which connects the gut to the brain, also chirped actively when there was fat in the gut of mice.
After identifying the biological mechanisms underlying the mouse’s preference for fat, Dr. Lee next took a closer look at the gut itself, specifically the endothelial cells that line the gut. She found her two groups of cells that send signals to vagus neurons in response to fat.
“One group of cells acts as a general sensor for essential nutrients, responding not only to fats, but also to sugars and amino acids,” says Dr. Li. “The other group responds only to fat, which may help the brain distinguish fat from other substances in the gut.”
Dr. Lee took another important step by using drugs to block the activity of these cells. Blocking signaling from either cell group prevented vagal neurons from responding to intestinal fat. She then used genetic techniques to inactivate either the vagus neurons themselves or neurons in the cNST. In both cases the mice lost their appetite for fat.
“These interventions confirm that each of these biological steps from the gut to the brain is important for the animal’s response to fat,” said Dr. Li.
“These experiments also provide new strategies for altering the brain’s response to fat and possibly its behavior to food.”
The stakes are high. Obesity rates have nearly doubled worldwide since 1980 he said. Today, nearly 500 million people suffer from diabetes.
“Excessive consumption of cheap, highly processed foods rich in sugar and fat is having a devastating impact on human health, especially among low-income and people of color communities.” said Dr. Zuker.
“The more we understand how these foods hijack the underlying biological mechanisms of taste and the gut-brain axis, the more opportunities we have to intervene.”
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Dr. Scott Sternson, professor of neuroscience at the University of California, San Diego, who wasn’t involved in the new research, emphasized its potential to improve human health.
“This exciting study provides insight into the molecules and cells that drive animals to crave fat,” said Dr. Sternson, whose research has focused on how the brain controls appetite. increase.
“Researchers’ ability to control this craving could ultimately lead to treatments that help combat obesity by reducing consumption of high-calorie, fatty foods.”
About this neuroscience and gut-brain axis research news
author: press office
sauce: Columbia University
contact: Press Office – Columbia University
image: Image credit goes to Mengtong Li / Zuker lab / Columbia’s Zuckerman Institute
Original research: closed access.
Mengtong Li, Hwei-Ee Tan, Zhengyuan Lu, Katherine S. Tsang, Ashley J. Chung, Charles S. Zuker, “The Fat-Preferring Gut-Brain Circuit”. Nature
Overview
Fat-loving gut-brain circuit
Perception of fat provokes a strong appetite and consumption response. Here we show that adipose stimulation can induce behavioral attraction even in the absence of a functional taste system. We show that fat acts post-ingestion via the gut-brain axis to promote fat preference.
Using single-cell data, we identified vagal neurons that respond to intestinal delivery of fat and showed that gene silencing of this gut-to-brain circuit abrogates the development of fat preference.
We then compared gut-to-brain pathways that prioritize fat over sugar, revealing two parallel systems. Activated only by fat stimulation.
Finally, we engineered animals lacking candidate receptors that detect the presence of intestinal fat and validated their role as mediators of gut-to-brain fat-evoked responses.
Together, these findings reveal distinct cells and receptors using the gut-brain axis as a fundamental conduit for the development of fat preference.
