A new animal study demonstrates one way sugar may contribute to metabolic diseases such as diabetes by causing disturbances in the gut microbiome. The new findings show exactly how certain gut bacteria can protect against the harmful effects of a high-fat diet, and how dietary sugar can disrupt these protective mechanisms.

It’s certainly not breaking news to suggest that a diet high in fat and sugar can lead to a variety of health problems. But as scientists learn more about the ways the trillions of bacteria in our gut can affect our overall health, we’re also gathering some unique insights into exactly how poor food choices cause certain health problems.

In this new study, the researchers first focused on what a high-fat, high-sugar diet did to the mice’s microbiome, focusing on a specific type of immune cell. Called Th17, these immune cells are a specialized subset of T cells that help protect the gut from certain pathogenic bacteria. Low levels of Th17 cells are associated with metabolic diseases and inflammatory conditions.

“These immune cells produce molecules that slow down the absorption of ‘bad’ lipids from the gut and reduce intestinal inflammation,” explained Ivaylo Ivanov, lead researcher of the project. “In other words, they keep the gut healthy and prevent the body from absorbing pathogenic lipids.”

So what happened to Th17 cells in the guts of mice when they were fed high-fat, high-sugar diets? Animals rapidly develop several features of metabolic disease (weight gain, glucose intolerance) and show a decrease in intestinal Th17 cells.

But more specifically, the researchers found that the reduction in Th17 levels was due to diet-induced changes in the gut microbiome. Bacteria known to promote Th17 were replaced by other types of gut bacteria. And sugar in particular appears to increase populations of harmful gut bacteria, which ultimately lower Th17 levels.

Interestingly, Ivanov said that while the animals maintained high levels of gut bacteria known to induce Th17, the high-fat diet did not lead to negative metabolic effects.

“Sugar eliminates the filamentous bacteria and as a result the protective Th17 cells disappear,” Ivanov said. “When we fed mice a sugar-free, high-fat diet, they retained intestinal Th17 cells and were completely protected from developing obesity and pre-diabetes, despite consuming the same number of calories.”

However, any metabolic health benefits obtained by removing sugar from the mouse diet were only evident in the presence of Th17-inducing gut bacteria. Without this specific microbial composition, animals on adjusted high-fat, low-sugar diets still gain weight and develop metabolic syndrome.

“This suggests that some popular dietary interventions, such as minimizing sugars, may only work in people who have certain bacterial populations in their microbiota,” Ivanov added.

According to Ivanov, some people may benefit from probiotics that help increase levels of Th17-inducing gut bacteria. But because mouse microbiomes are different from humans, it’s unclear exactly what types of bacteria would be optimal, and even with that knowledge, a targeted probiotic would only be useful in scenarios where clinicians can be sure a person will need it. of these particular microbes.

Perhaps the most obvious takeaway from the findings is that one way dietary sugar can lead to metabolic problems is by altering Th17 levels in the gut. And Ivanov speculates a future in which Th17 is directly therapeutically targeted, rather than trying to modulate bacterial mediators.

“Our study highlights that the complex interplay between diet, microbiota and the immune system plays a key role in the development of obesity, metabolic syndrome, type 2 diabetes and other conditions,” Ivanov said. “This suggests that for optimal health, it is important not only to change your diet, but also to improve your microbiome or gut immune system, for example by increasing Th17 cell-inducing bacteria.”

The new study is published in cell.

source: Columbia University Irving Medical Center


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