The findings, published in the U.S. journal Science, demonstrate the transmission of physical and metabolic traits via gut microbes, representing an important step toward the ultimate goal of developing anti-obesity treatment with bacteria.
Researchers from the Washington University recruited four human twin pairs discordant for obesity and transferred the gut microbiota in fecal samples from each of them into the guts of germ-free mice that had been raised under sterile conditions, without any microbes of their own.
They found that the recipients of the obese twins’ microbiota gained more fat than the recipients of the lean twins’ microbiota if the mice are fed a standard diet.
“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. Our question became: What were the components responsible?” said Jeffrey Gordon, director for the Center of Genome Sciences and Systems Biology at Washington University School of Medicine and a co-author of the paper.
When the researchers housed mice receiving microbes from a lean twin with mice given microbes from an obese twin for five days, they discovered that the obese mice slimmed down but the lean mice appeared unaffected.
Analysis of the bacterial communities showed that specific members of the so-called Bacteroidetes phylum could pass from the lean mice and colonize the obese mice, suggesting that these bacteria were largely responsible for protection against weight gain.
According to the researchers, none of the bacteria from the obese mice could invade the lean mice to make them accumulate fat.
To learn more, the researchers formulated diets for the mice that were representative of modern Western diets — low in fiber and high in saturated fats — and found both the obese and lean mice appeared to be unaffected by the others’ gut microbes.
However, when the animals were given the “healthier”, high- fiber and low-fat human diet, the results were the same as before.
The findings indicated that more complex interactions between diet, body mass and gut microbiota underlie human metabolic disturbances than researchers have appreciated.
“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 the future, the nutritional value and the effects of food will involve significant consideration of our microbiota — and developing healthy, nutritious foods will be done from the inside- out, not just the outside-in,” he said.