Bacteria
from Lean Humans Can Slim Obese Mice
A
new study suggests that more complex interactions between diet, body mass, and
gut microbiota underlie metabolic disturbances than previously thought.
·
Patricia
Fitzpatrick Dimond, Ph.D.
Graduate student Vanessa Ridaura and colleagues
at the Center for Genome Sciences and Systems Biology,University of
Washington School
of Medicine reported in the September 6 issue of Science that mice lacking
bacterial colonies of their own that received gut bacteria from obese humans
put on more weight and accumulated more fat than mice that were given bacteria
from the guts of lean humans.
To directly test the influence of the human gut microbiome on obesity, the
investigators sampled microbes living in the guts of human fraternal and
identical twins, one of whom was lean while the other, obese. They introduced
these microbes into germ-free mice fed low-fat mouse chow, as well as diets
representing different levels of saturated fat and fruit and vegetable
consumption typical of the U.S.
diet. Increased total body and fat mass, as well as obesity-associated
metabolic phenotypes, were transmissible with uncultured fecal communities and
with their corresponding fecal bacterial culture collections.
“The first thing that Vanessa identified in
these mice, which were consuming a standard mouse diet, was that the recipients
of the obese twins' microbiota gained more fat than the recipients of the lean
twins' microbiota,” Jeffrey Gordon, M.D., director of the Center and a
co-author of the Science report, explained. Since, he said, the differences
could not be attributed to the amount of food the mice consumed, “there was
something in the microbiota that was able to transmit this trait. Our question
became: What were the components responsible?"
To perform what Dr. Gordon called “The Battle of
the Microbiota,” the investigators housed mice that had received microbes from
a lean twin (Ln mice) with mice that were given microbes from an obese twin (Ob mice). “Mice—delicately put—exchange their microbes
readily,” said Dr. Gordon, referring to coprophagia, or the consumption of
feces.
When Ridaura and her colleagues housed Ln mice
with Ob mice for 10 days, they discovered that the Ob mice—affected by their
cage mates’ microbes—slimmed down, adopting the “leaner” metabolism of the Ln
mice. Ln mice, on the other hand, appeared unaffected and maintained their own
metabolism, they say. The “rescue” of mice from obesity was correlated with
colonization of specific members of Bacteroidetes bacteria that were part of the
Ln biota, and, importantly, was diet-dependent. Only those mice eating a
low-saturated fat, high fruit and vegetable diet became colonized with the
Ln–associated bacteria. These animals did not become obese.
These findings suggest that more complex
interactions between diet, body mass, and gut microbiota underlie human
metabolic disturbances than previously understood. The mouse models employed by investigators could be
used to identify other aspects of how the human gut microbiota and our diets
influence human health.
“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,” said Dr. Gordon. “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.”
The study appears in the September 6 issue of
Science with the title, “Gut Microbiota from Twins Discordant for Obesity
Modulate Metabolism in Mice”.
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