Can Gut Bugs Make You Fat? Or Skinny?
Published: Sep 7, 2013, By Kristina Fiore, Staff Writer, MedPage Today, Reviewed by Robert Jasmer, MD; Associate Clinical Professor of Medicine, University of California, San Francisco
Transplanting intestinal bacteria from lean or obese humans can turn mice fat or thin, and diet may transform that phenotype, researchers found.
In a series of studies using fecal material from pairs of obese and lean twins, mice given bacteria from the heavier twin gained more weight and packed on more adipose tissue than mice given bacteria from the thin twin (P?0.01), Jeffrey Gordon, MD, of Washington University in St. Louis, and colleagues reported in Science.
There was also evidence of bacterial sharing when these mice were housed together, and the lean mice appeared to confer protective benefits to their obese counterparts. That effect was facilitated by a healthy, low-saturated-fat, high-fiber diet, but was stymied by an unhealthy one full of saturated fats and short on fiber, Gordon and colleagues reported.
"We now have a way of identifying such interactions, dependent on diet, and thinking about what features of our unhealthy diets we could transform in ways that would encourage bacteria to establish themselves in our guts, and do the jobs needed to improve our well-being," Gordon said in a statement.
Much research has focused on the effects of the intestinal microbiome and its effects on human obesity. Recent findings from the MetaHIT project in Europe have shown that these 'gut bugs' have a great impact on metabolic health.
For instance, Danish patients with less diversity of intestinal bacteria were found to have more metabolic dysfunction than those with a more robust portfolio. Another study reported at the same time found that healthier diets improved the number and types of intestinal bacteria.
For their study, Gordon and colleagues took fecal material from pairs of adult female twins -- one who was obese, the other lean -- and transplanted it into mice that were bred to have no intestinal bacteria at all. All of these mice were given a standard diet that was low in fat and high in plant polysaccharides.
The researchers found that mice given bacteria from the heavier twin gained more weight and accumulated more adipose tissue than those who received intestinal bacteria from the leaner twin (P?0.01).
"This wasn't attributable to differences in the amount of food they consumed, so there was something in the microbiota that was able to transmit this trait," Gordon said in the statement. "Our question became: What were the components responsible?"
So they placed the mice together, an easy way of sharing intestinal bacteria because mice engage in coprophagia, the consumption of feces.
After living together for 10 days, the researchers found the obese mice had adopted features of their leaner cage mates, packing on less adiposity than obese animals not housed with lean mice (P?0.05). At the same time, exposure to the obese mice didn't make the lean animals fat.
Specifically, the obese mice gained bacteria in the genus Bacteroides, which has been associated with less obesity in previous work.
To assess whether a change in diet would have an impact on these effects, Gordon and colleagues put the mice on two different diets: a healthy one that was low in saturated fats and high in fiber, and another that was the opposite -- high in saturated fat and low in fiber.
They found that among animals on the healthier diet, lean mice were still able to confer metabolic benefits to their obese counterparts, via an invasion of Bacteroides. But the high-fat, low-fiber diet stymied that benefit, and obese animals housed with lean ones gained no benefits, they reported.
"Remarkably, there was a lack of significant invasion of members of the lean microbiota into the guts of obese cage mates," the researchers wrote. "Together, these results emphasize the strong microbiota-by-diet interactions that underlie invasion, and illustrate how a diet high in saturated fats and low in fruits and vegetables can select against human gut bacterial taxa associated with leanness."
Gordon and colleagues concluded that their findings suggest complex interactions between diet, body mass, and gut microbiota underlie metabolic dysfunction, and that their model will be useful for future studies looking at the effects of specific dietary components on intestinal bacteria and subsequent phenotypes.
"In the future, the nutritional value and the effects of food will involve significant consideration of our microbiota," Gordon said, "and developing healthy, nutritious foods will be done from the inside-out, not just the outside-in."
The study was supported by the National Institutes of Health, the Crohn's and Colitis Foundation of America, Kraft Foods, and Mondelez International.