CERTAIN GUT BACTERIA MAY INDUCE METABOLIC CHANGES FOLLOWING EXPOSURE TO ARTIFICIAL SWEETENERS TNERESW
Artificial sweeteners
-- promoted as aids to weight loss and diabetes prevention -- could actually
hasten the development of glucose intolerance and metabolic disease, and they
do so in a surprising way: by changing the composition and function of the gut microbiota
-- the substantial population of bacteria residing in our intestines. These
findings, the results of experiments in mice and humans, were published
September 17 in Nature. Dr.
Eran Elinav of the Weizmann Institute of Science's Department of Immunology,
who led this research together with Prof. Eran Segal of the Department of
Computer Science and Applied Mathematics, says that the widespread use of
artificial sweeteners in drinks and food, among other things, may be
contributing to the obesity and diabetes epidemic that is sweeping much of the
world
For years, researchers
have been puzzling over the fact that non-caloric artificial sweeteners do not
seem to assist in weight loss, with some studies suggesting that they may even
have an opposite effect. Graduate student Jotham Suez in Dr. Elinav's lab, who
led the study, collaborated with lab member Gili Zilberman-Shapira and graduate
students Tal Korem and David Zeevi in Prof. Segal's lab to discover that
artificial sweeteners, even though they do not contain sugar, nonetheless have
a direct effect on the body's ability to utilize glucose. Glucose intolerance
-- generally thought to occur when the body cannot cope with large amounts of
sugar in the diet -- is the first step on the path to metabolic syndrome and
adult-onset diabetes.
The scientists gave
mice water laced with the three most commonly used artificial sweeteners, in
amounts equivalent to those permitted by the U.S. Food and Drug Administration
(FDA). These mice developed glucose intolerance, as compared to mice that drank
water, or even sugar water. Repeating the experiment with different types of mice
and different doses of the artificial sweeteners produced the same results --
these substances were somehow inducing glucose intolerance.
Next, the researchers
investigated a hypothesis that the gut microbiota are involved in this
phenomenon. They thought the bacteria might do this by reacting to new
substances like artificial sweeteners, which the body itself may not recognize
as "food." Indeed, artificial sweeteners are not absorbed in the
gastrointestinal tract, but in passing through they encounter trillions of the
bacteria in the gut microbiota.
The researchers
treated mice with antibiotics to eradicate many of their gut bacteria; this
resulted in a full reversal of the artificial sweeteners' effects on glucose
metabolism. Next, they transferred the microbiota from mice that consumed
artificial sweeteners to "germ-free," or sterile, mice -- resulting
in a complete transmission of the glucose intolerance into the recipient mice.
This, in itself, was conclusive proof that changes to the gut bacteria are
directly responsible for the harmful effects to their host's metabolism. The
group even found that incubating the microbiota outside the body, together with
artificial sweeteners, was sufficient to induce glucose intolerance in the
sterile mice. A detailed characterization of the microbiota in these mice
revealed profound changes to their bacterial populations, including new
microbial functions that are known to infer a propensity to obesity, diabetes,
and complications of these problems in both mice and humans.
Does the human
microbiome function in the same way? Dr. Elinav and Prof. Segal had a means to
test this as well. As a first step, they looked at data collected from their
Personalized Nutrition Project ,the largest human trial to date to look at the
connection between nutrition and microbiota. Here, they uncovered a significant
association between self-reported consumption of artificial sweeteners,
personal configurations of gut bacteria, and the propensity for glucose
intolerance. They next conducted a controlled experiment, asking a group of
volunteers who did not generally eat or drink artificially sweetened foods to
consume them for a week, and then undergo tests of their glucose levels and gut
microbiota compositions.
The findings showed
that many -- but not all -- of the volunteers had begun to develop glucose
intolerance after just one week of artificial sweetener consumption. The
composition of their gut microbiota explained the difference: the researchers
discovered two different populations of human gut bacteria -- one that induced
glucose intolerance when exposed to the sweeteners, and one that had no effect
either way. Dr. Elinav believes that certain bacteria in the guts of those who
developed glucose intolerance reacted to the chemical sweeteners by secreting
substances that then provoked an inflammatory response similar to sugar overdose,
promoting changes in the body's ability to utilize sugar.
Prof. Segal states,
"The results of our experiments highlight the importance of personalized
medicine and nutrition to our overall health. We believe that an integrated
analysis of individualized 'big data' from our genome, microbiome, and dietary
habits could transform our ability to understand how foods and nutritional
supplements affect a person's health and risk of disease."
According to Dr.
Elinav, "Our relationship with our own individual mix of gut bacteria is a
huge factor in determining how the food we eat affects us. Especially
intriguing is the link between use of artificial sweeteners -- through the
bacteria in our guts -- to a tendency to develop the very disorders they were
designed to prevent; this calls for reassessment of today's massive,
unsupervised consumption of these substances."
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