Digestive microbes affect overeating of sweet treats
Digestive microbes affect overeating of sweet treats
Abstract: A lack of certain gut bacteria causes mice to overeat sweet, palatable food. When the bacteria recovers, cravings for sugary foods diminish and normal eating patterns resume.
You just meant to eat one Oreo as a snack, but then you go back for another, and another, and before you know it, you’ve eaten 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: maybe it’s not entirely your fault. Now, new research in mice shows that certain gut bacteria can suppress overeating.
Oreos and other desserts are examples of so-called “palatable foods”—foods that are consumed for hedonic pleasure rather than simply for hunger or nutritional needs. Humans aren’t the only ones who enjoy this kind of hedonism: mice like to eat dessert, too. Even when they have just eaten, they will still consume sweet snacks if they are available.
A new Caltech study shows that the absence of certain gut bacteria causes mice to overeat palatable food: Mice with microbiota disrupted by oral antibiotics consumed 50% more sugar balls over two hours than mice with gut bacteria. When their microbiota was restored by fecal transplants, the mice returned to their normal feeding pattern.
Furthermore, not all gut bacteria are able to suppress hedonic feeding, but certain species appear to alter the behavior. Binge eating is only about tasty food; mice with or without gut microbiota still eat the same amount of their regular diet.
The findings show that the gut microbiota has an important influence 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 laboratory of Sarkis Mazmanian, Luis B. and Nelly Soux, professor of microbiology.
A paper 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 realization that motivation-driven feeding behavior is governed by the composition of the gut microbiome has implications not only for obesity, diabetes, and other metabolic conditions, but perhaps also for excessive use of alcohol, nicotine, or illicit pleasure-producing substances. “
To examine how the gut microbiota affects feeding behavior, Ousey gave a group of mice antibiotics for four weeks, destroying the animals’ gut bacteria. He then compared their eating behavior with normal mice with healthy gut microbiota. The two groups ate roughly the same amount of their standard mouse diet, called chow.
But the real difference was how much palatable or dessert-like food the mice consumed. When given high-sucrose pellets, the antibiotic-treated mice ate 50% more pellets over two hours and ate in longer bursts than their healthy counterparts.
Ousey then tried to determine how much effort the mice were willing to put in to get sugary snacks. In another set of experiments, instead of simply placing treats in their cages, the mice had to press a button to get a pellet. Each successive ball required the mice to press the button more and more times.
Untreated mice would at some point lose interest in pressing the button and wander off. However, mice given oral antibiotics made much more effort 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 the mice to normal feeding behavior simply by restoring the mouse microbiota via fecal transplantation. Mice that recovered still consumed sugar when it was available, but did not show the same binge eating behavior.
The digestive microbiota contains hundreds of bacterial species, and the team suspected that some were more influential than others in promoting overeating.
“To find out which microbes might be involved, I gave different cohorts of mice different antibiotics individually,” explains Ousey.
“Different antibiotics target different bacteria. What I noticed 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 some microbe, or some collection of microbes, that is sensitive to ampicillin or vancomycin, that is responsible for controlling the normal response to highly palatable foods.”
The team then found that increased levels of bacteria from the S24-7 family (a type of bacteria specific to lab mice) and from the genus Lactobacillus were associated with reduced overeating. When these bacterial species were given to mice treated with antibiotics, but not other bacteria, hedonic feeding was suppressed.
Although the study only draws conclusions about the mice’s microbiota, it opens up new lines of study to understand how and why we can be driven to overconsume sugary snacks.
“I think it would be very intriguing to see if people who receive oral antibiotics show differences in their eating patterns and food choices and if these things can be linked to the gut microbiota,” says Ousey.
“We know that people with eating disorders such as binge eating disorder and anorexia nervosa have differences in their gut microbiota compared to people not diagnosed with these conditions.
“Obviously, maybe an eating disorder affects the microbiota because they’re eating different foods; maybe it’s a two-way street. But research into how antibiotics might affect people’s responses to palatable food is definitely feasible.”
“We do not understand the neurobiology underlying the observation that the microbiome influences the overconsumption of palatable food in mice,” says Mazmanian.
“Future studies in our lab and others will explore the gut-brain axis in the modulation of reward circuits in the brain, as well as the possible design of probiotics for intervention in eating disorders.”
About this microbiome and nutrition research news
Author: Lori Dajose
Contact: Lori Dajose – CalTech
Picture: The image is in the public domain
Original research: Open access.
“Gut microbiota suppress feeding induced by palatable food” by James Ousey et al. Current Biology
Gut microbiota suppress feeding induced by palatable food
- Depletion of the intestinal microbiota of mice reversibly results in excessive consumption of palatable food
- Microbiota-depleted mice show greater motivation to seek a high-sucrose reward
- Colonization with S24-7 i L. johnsonii reduces vancomycin-induced binge eating
Feeding behavior depends on internal and external factors including genetics, food taste and environment.
Gut microbiota is a major environmental factor in host physiology and influences feeding behavior.
Here, we investigated the hypothesis that gut bacteria influence behavioral responses to palatable food and find that antibiotic depletion (ABX) of gut microbiota in mice results in overconsumption of several palatable foods with preserved effects on feeding dynamics.
Restoration of intestinal microbiota via fecal transplantation in ABX mice is sufficient to rescue excessive consumption of high-sucrose pellets.
Operant conditioning tests revealed that ABX mice showed increased motivation to seek high-sucrose rewards. Accordingly, neuronal activity in the mesolimbic regions of the brain, which is associated with motivation and reward-seeking behavior, was elevated in ABX mice after consuming high-sucrose pellets.
Differential antibiotic treatment and functional microbiota transplants identified specific taxa of gut bacteria from the S24-7 family and genus Lactobacillus whose abundance is associated with suppression of the consumption of pellets with a high sucrose content.
Indeed, colonization of mice with S24-7 i Lactobacillus johnsonii was sufficient to reduce excessive consumption of high-sucrose pellets in an antibiotic-induced binge eating model.
These results indicate that external influences from the gut microbiota can suppress the behavioral response to palatable food in mice.
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