Summary: The absence of certain intestinal bacteria causes mice to gorge on sugary and appetizing foods. When the bacteria is restored, the desire to binge on sweet foods decreases and normal eating habits resume.
You just wanted to grab a single Oreo as a snack, but then you find yourself coming back for another, and another, and before you know it, you’ve finished the whole package even though you weren’t that hungry to begin with. .
But before you start feeling too guilty about your gluttony, consider this: it might not be entirely your fault. Now, new research in mice shows that specific gut bacteria can suppress binge eating behavior.
Oreos and other desserts are examples of so-called “tasty foods” – foods eaten for hedonistic pleasure, not simply for hunger or nutritional need. Humans aren’t the only ones who enjoy this kind of hedonism: mice also like to eat desserts. Even when they have just eaten, they will continue to consume sugary snacks if they are available.
New Caltech Study Shows Lack of Certain Gut Bacteria Causes Mice to Eat Appetizing Foods: Mice Whose Microbiota Disrupted by Oral Antibiotics Consumed 50% More Sugar Pellets in Two Hours Than Mice with intestinal bacteria. When their microbiota was restored by fecal transplants, the mice returned to normal eating behavior.
Additionally, not all gut bacteria are able to suppress hedonic feeding, but rather specific species appear to modify behavior. Binging only applies to tasty foods; mice with or without gut microbiota always eat the same amount of their usual diet.
The results show that the gut microbiota has important influences on behavior and that these effects can be modulated when the microbiota is manipulated.
The study was led by graduate student James Ousey in the lab of Sarkis Mazmanian, Luis B. and Nelly Soux Professor of Microbiology.
An article describing the research appears in the journal Current biology November 29.
“The gut microbiome has been shown to influence many behaviors and disease states in mouse models, from sociability and stress to Parkinson’s disease,” says Mazmanian.
“The recent appreciation that motivational-driven eating behaviors are subject to the composition of the gut microbiome has implications not only for obesity, diabetes, and other metabolic conditions, but possibly for the overconsumption of alcohol, nicotine or illicit substances that provide pleasure.”
To examine how the gut microbiota influenced eating behaviors, Ousey gave a group of mice antibiotics for four weeks, killing the animals’ gut bacteria. He then compared their eating behavior to that of normal mice with a healthy gut microbiota. Both groups ate roughly the same amount of their standard mouse diet, called chow.
But the real difference was in how much appetizing, or dessert-like, food the mice ate. When given the high-sucrose pellets, the antibiotic-treated mice ate 50% more pellets in two hours and ate longer than their healthy mouse counterparts.
Ousey then set out to determine how much effort the mice were willing to put in to get sweet snacks. In another set of experiments, instead of just having treats placed in their cages, the mice had to press a button to receive a pellet. Each subsequent pellet made the mice press the button more and more times.
Untreated mice, at some point, would lose interest in pressing the button and walk away. However, the mice given oral antibiotics worked much harder to get more and more sugar, pressing the button repeatedly as if they were desperate for a snack.
Importantly, this binge-eating behavior is actually reversible: researchers could return mice to normal eating behavior simply by restoring the mouse’s microbiota through a fecal transplant. The restored mice still consumed sugar when available but did not exhibit the same overeating behavior.
The gut microbiota contains hundreds of bacterial species, and the team suspected that some were more influential than others in driving binge eating behavior.
“To determine which specific microbes might be involved, I gave different antibiotics to different cohorts of mice individually,” says Ousey.
“Different antibiotics target different bacteria. What I observed was that mice given ampicillin or vancomycin, but not neomycin or metronidazole, overconsumed these high sucrose pellets compared to controls.
“This would suggest that there is a microbe, or collection of microbes, sensitive to ampicillin or vancomycin that is responsible for controlling the normal response to highly palatable foods.”
The team then identified that increased levels of bacteria from the S24-7 family (a type of bacteria specific to lab mice) and the Lactobacillus genus were associated with reduced overconsumption. When these bacterial species were fed to the antibiotic-treated mice, but not to other bacteria, hedonic feeding was suppressed.
Although the study only draws conclusions about the microbiota of mice, it opens up new avenues of study to understand how and why we may overconsume sugary snacks.
“I think it would be so intriguing to see if people receiving oral antibiotics show any differences in their eating habits and food choices, and if those things might be associated with gut microbiota,” Ousey says.
“We know that humans with eating disorders like binge eating disorder and anorexia nervosa have differences in their gut microbiota compared to humans who are not diagnosed with these conditions.
“Obviously, maybe the eating disorder affects the microbiota because they eat different foods; it may be two-way. But investigations into how antibiotics might affect responses to appetizing foods in humans are certainly doable.
“We don’t understand the neurobiology underlying the observation that the microbiome impacts the overconsumption of appetizing foods in mice,” Mazmanian says.
“Future studies in our lab and others will explore the gut-brain axis by modulating reward circuitry in the brain and possibly designing probiotics to intervene in eating disorders.”
About this microbiome and food research news
Author: Lori Dajosé
Contact: Lori Dajose – CalTech
Image: Image is in public domain
Original research: Free access.
“Gut Microbiota Suppress Tasty Food Induced Eating” by James Ousey et al. Current biology
Gut microbiota suppress appetizing food-induced feeding
- Depletion of gut microbiota in mice reversibly leads to overconsumption of palatable foods
- Microbiota-depleted mice exhibit greater motivation to seek sucrose-rich reward
- Colonization with S24-7 and L. johnsonii reduces vancomycin-induced binge eating
Eating behaviors depend on intrinsic and extrinsic factors, including genetics, food palatability, and environment.
The gut microbiota is a major environmental contributor to host physiology and impacts feeding behavior.
Here, we explored the hypothesis that gut bacteria influence behavioral responses to appetizing foods and reveal that antibiotic depletion (ABX) of the gut microbiota in mice leads to overconsumption of multiple appetizing foods with retained effects on the dynamics of food.
Restoration of gut microbiota by fecal transplantation in ABX mice is sufficient to rescue overconsumption of high sucrose pellets.
Operant conditioning tests revealed that ABX mice exhibit increased motivation to seek sucrose-rich rewards. As a result, neural activity in mesolimbic brain regions, which have been linked to motivation and reward-seeking behavior, was elevated in ABX mice after consumption of high-sucrose pellets.
Differential antibiotic treatment and functional microbiota transplants identified specific gut bacterial taxa of the S24-7 family and genus Lactobacillus the abundance of which is associated with the elimination of the consumption of pellets with a high sucrose content.
Indeed, colonization of mice with S24-7 and Lactobacillus johnsonii was sufficient to reduce overconsumption of high-sucrose pellets in an antibiotic-induced binge eating model.
These results demonstrate that extrinsic influences of the gut microbiota can suppress the behavioral response to appetizing foods in mice.
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