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High-sugar diet disrupts the gut microbiome, resulting in obesity (in mice)

illustration of cells lining the gut with multi-colored gut bacteria on their surfaces

Specific bacteria in the mouse gut help protect the rodents from metabolic disease.(Image credit: NANOCLUSTERING/SCIENCE PHOTO LIBRARY via Getty Images)

Sugar may disrupt the city of bacteria surviving in the gut, thereby depleting crucial immune cells and causing obesity down the road, a fresh mouse study suggests.

Up to now, the results have already been shown only in mice. But if follow-up studies also show similar trends in humans, which could eventually result in treatments for metabolic disease and obesity, said senior author Ivaylo Ivanov, a co-employee professor of microbiology and immunology at Columbia University Vagelos College of Physicians and Surgeons.

In the recent study, published online Aug. 29 in the journal Cell (opens in new tab), scientists discovered that feeding mice a high-sugar diet containing sucrose and maltodextrin caused specific bacteria, called segmented filamentous bacteria (SFB), in the mice’s intestines to die because of an overgrowth of different gut bugs. The sudden lack of SFB triggered a chain reaction in the mouse gut that ultimately changed the way the animals absorbed fat molecules.

This, subsequently, caused the mice to become obese and develop top features of “metabolic syndrome,” a cluster of conditions such as for example raised blood pressure, high blood sugar levels and insulin resistance that collectively improve the threat of cardiovascular disease, stroke and type 2 diabetes.

Related: Gut bacteria may ‘talk’ to the mind, mouse study suggests

The outcomes claim that SFB somehow drive back metabolic syndrome and unwanted weight gain, but just how do the gut bugs take action? As it happens that SFB “talk” to the disease fighting capability, encouraging the production of a particular kind of immune cell called Th17. These immune cells release proteins that affect the liner of the intestine, preventing surplus fat from being absorbed through the tissue and in to the bloodstream.

Broadly, SFB are available in many animals including rodents, fish and birds however they haven’t been within humans, Ivanov noted. However, humans do carry another group of gut bacteria that may induce Th17 cells exactly like SFB do, and early research hints (opens in new tab) these bacteria could be similarly depleted by high-sugar diets, he said. Basically, although humans might not carry SFB, sugar may still exert similar effects on the mouse and human gut microbiomes and immune systems.

“Really what’s providing the result may be the T cells therefore the bacteria are causing the T cells, and T cells are providing the result,” Ivanov told Live Science. “We hypothesize that, in humans, inducing these T cells may also be beneficial.”

Within their recent mouse study, the researchers placed mice on a high-sugar, high-fat diet for per month to observe how their gut bugs might change. They discovered that the dietary plan spurred the growth of a bacterium called Faecalibaculum rodentium, which essentially crowded out the SFB growing in the mouse gut, depleting its numbers. Because the mice steadily lost SFB, their overall amount of Th17 cells also fell, plus they gained weight and developed insulin resistance and glucose intolerance all signs of metabolic syndrome.

These effects weren’t seen in mice which were fed a low-sugar, low-fat diet, or in mice fed a sugar-free, high-fat diet, but mice fed a high-sugar, low-fat diet also swiftly lost their SFB. This shows that it had been specifically the sugar that has been driving the harmful lack of the bacteria and the Th17 cells.

Basically, the Th17 cells provided an “armor” that protected the mice from developing metabolic disease, and sugar indirectly destroyed that armor by messing with the microbiome, Ivanov explained.

In another experiment, the team eliminated SFB from the band of mice and fed them a sugar-free, high-fat diet. They discovered that these mice also gained weight and developed metabolic disease, despite devoid of eaten sugar. Just what exactly gives? Essentially, minus the right gut bugs, the mice didn’t make enough Th17 cells plus they thus lacked that aforementioned armor. The team discovered that they might provide that armor in two ways: by feeding the mice a probiotic imbued with SFB or by directly injecting Th17 cells to their bodies.

This shows that, in case a mouse’s gut was already depleted of SFB, reducing sugar won’t help the rodent avoid metabolic disease. If this finding carries to humans, that shows that eating less sugar wouldn’t necessarily be helpful if one’s gut microbiome has already been disrupted. Therefore, yet another intervention may be had a need to restore the gut bugs or Th17 cells of these people, Ivanov said.

Again, more research is required to know if similar forces are in work in the human gut. Ivanov and his team may also be trying to know how gut bacteria help Th17 cells grow in the mouse gut and whether that mechanism also applies in humans.

“Even with 10 years of studying this, we hardly understand completely this technique, this mechanism, how the bacteria is inducing these T cells,” Ivanov said. “We realize a lot, but nonetheless there are a great number of questions.”

Originally published on Live Science.

Nicoletta Lanese is really a staff writer for Live Science covering health insurance and medicine, alongside a variety of biology, animal, environment and climate stories. She holds degrees in neuroscience and dance from the University of Florida and a graduate certificate in science communication from the University of California, Santa Cruz. Her work has appeared in The Scientist Magazine, Science News, The San Jose Mercury News and Mongabay, among other outlets.

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