Sugar can alter the community of bacteria living in the gut, thereby depleting crucial immune cells and causing obesity, a new mouse study suggests.
So far, the results have only been shown in mice. But if follow-up studies show similar trends in humans, it could lead to treatments for metabolic diseases and obesity, said lead author Ivaylo Ivanov, associate professor of microbiology and immunology at the Vagelos College of Physicians and Surgeons of the Columbia University.
In the recent study, published online August 29 in the journal cell (opens in a new tab)scientists found that feeding mice a high-sugar diet containing sucrose and maltodextrin caused bacteria, called segmented filamentous bacteria (SFB), in the intestines of mice to die from an overgrowth of different intestinal bugs. The sudden loss of SFB set off a chain reaction in the mouse gut that ultimately changed how the animals absorbed. dietary fat.
This, in turn, caused the mice to become obese and develop features of “metabolic syndrome,” a set of conditions including high blood pressure, high blood sugar, and insulin resistance — which collectively increase the risk of heart diseasestroke and type 2 diabetes.
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The results suggest that SFB somehow protects against metabolic syndrome and excess weight, but how do gut bugs do it? It turns out that SFB “talks” to the immune system, encouraging the production of a specific type of immune cell called Th17. These immune cells release proteins that affect the lining of the intestine, preventing excess fat from being absorbed through the tissue and into the bloodstream.
Broadly speaking, SFB can be found in many animals, including rodents, fish and birds, but has not been found in humans, Ivanov noted. However, humans carry a different set of gut bacteria that can induce Th17 cells just as SFB does, and first research leads (opens in a new tab) that these bacteria can be similarly depleted by high-sugar diets, he said. In other words, even though humans may not carry SFB, sugar can still exert similar effects on mouse and human gut microbiomes and immune systems.
“What’s really providing the effect is the T cells, so the bacteria are inducing the T cells and the T cells are providing the effect,” Ivanov told Live Science. “We hypothesize that in humans, inducing these T cells will also be beneficial.”
In their recent mouse study, researchers placed mice on a high-sugar, high-fat diet for a month to see how their gut bugs might change. They discovered that the diet stimulated the growth of a bacteria called Rodent droppings, which essentially eliminated the SFB growing in the mouse intestine, depleting their numbers. As the mice steadily lost SFB, their total number of Th17 cells also fell, and they gained weight and developed insulin resistance and glucose intolerance, all signs of metabolic syndrome.
These effects were not seen in mice 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 they lost quickly. his SFB. This suggests that it was specifically the sugar that caused the harmful loss of bacteria and Th17 cells.
Basically, Th17 cells provided “armor” that protected the mice from developing metabolic diseases, and sugar indirectly destroyed that armor by interfering with the microbiome, Ivanov explained.
In a separate experiment, the team removed SFB from a group of mice and then fed them a high-fat, sugar-free diet. They found that these mice also gained weight and developed metabolic disease, despite not eating sugar. So what gives? Essentially, without the right gut bugs, the mice didn’t make enough Th17 cells and therefore lacked that aforementioned armor. The team found that they could provide this armor in two ways: by feeding the mice a SFB-infused probiotic or by directly injecting Th17 cells into their bodies.
This suggests that if a mouse’s gut is already depleted of SFB, reducing sugar will not help the rodent avoid metabolic disease. If this finding translates to humans, it suggests that consuming less sugar would not necessarily be helpful if the gut microbiome is already disrupted. Therefore, additional intervention might be needed to restore gut bugs or Th17 cells in these people, Ivanov said.
Again, more research is needed to know if similar forces are at work in the human gut. Ivanov and his team are also trying to understand how gut bacteria help Th17 cells grow in the mouse gut and whether this mechanism also applies to humans.
“Even after 10 years of studying it, we don’t fully understand this process, this mechanism, how exactly the bacteria induce these T cells,” Ivanov said. “We know a lot, but there are still a lot of questions.”
Originally published in Live Science.