Artificial sweeteners linked to diabetes, obesity

Scientists have found that after exposure to artificial sweeteners our gut bacteria may be triggering harmful metabolic changes that can lead to diabetes and obesity.
Researchers from the Weizmann Institute of Science in Israel discovered that artificial sweeteners, even though they do not contain sugar, nonetheless have a direct effect on the body's ability to utilise 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.
Researchers in the new study gave mice water laced with the three most commonly used artificial sweeteners, in amounts equivalent to those permitted by the US 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 recognise as "food."
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.
A detailed characterisation 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.
Researchers also conducted a controlled experiment in humans, 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.
Researchers believe 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 utilise sugar.