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Gut bacteria

Gut bacteria prevent mice from developing obesity

Results from this study showed that Clostridia prevents weight gain by blocking the intestine's ability to absorb fat

Researchers at University of Utah Health have identified a specific class of bacteria from the gut that prevents mice from becoming obese, suggesting these same microbes may similarly control weight in people. The beneficial bacteria, called Clostridia, are part of the microbiome - collectively trillions of bacteria and other micro-organisms that inhabit the intestine.

The study, ‘T cell–mediated regulation of the microbiota protects against obesity’, published in Science shows that healthy mice have plenty of Clostridia - a class of 20 to 30 bacteria - but those with an impaired immune system lose these microbes from their gut as they age. Even when fed a healthy diet, the mice inevitably become obese. Giving this class of microbes back to these animals allowed them to stay slim.

"Now that we've found the minimal bacteria responsible for this slimming effect, we have the potential to really understand what the organisms are doing and whether they have therapeutic value," said Dr June Round, an associate professor of pathology at U of U Health, the study's co-senior author.

Mice that inevitably become obese have a compromised immune system and less of a class of bacteria called Clostridia in their gut microbiome than healthy mice. Giving Clostridia to the immune-impaired mice prevents obesity (Credit: Luat Nguyen, University of Utah Health)

Results from this study showed that Clostridia prevents weight gain by blocking the intestine's ability to absorb fat. Mice experimentally treated so that Clostridia were the only bacteria living in their gut were leaner with less fat than mice that had no microbiome at all. They also had lower levels of a gene, CD36, that regulates the body's uptake of fatty acids.

These insights could lead to a therapeutic approach, Round says, with advantages over the faecal transplants and probiotics that are now being widely investigated as ways to restore a healthy microbiota. Therapeutics such as these, that are based on transferring living microbiome to the gut, won't work for everyone due to differences in diet and other factors that influence which bacteria can survive and thrive.

The current study found that one or more molecules produced by Clostridia prevented the gut from absorbing fat. The next step is to isolate these molecules and further characterize how they work to determine whether they could inspire focused treatments for obesity, type 2 diabetes, and other related metabolic disorders.

A beneficial class of bacteria, called Clostridia, prevents mice with a compromised immune system from becoming obese (Credit: Charlie Ehlert, University of Utah Health)

"These bacteria have evolved to live with us and benefit us," said Dr Charisse Petersen, a graduate student at the time, led the research. "We have a lot to learn from them."

Finding that mice with a compromised immune system could not help but become obese was a discovery that almost didn't happen. Serendipity brought Petersen into the lab at the right time to see that mice genetically engineered to lack myd88, a gene central to the immune response, were "as fat as pancakes." She had let the rodents age longer than usual, revealing an unappreciated link between immunity and obesity.

Still, the observation didn't answer the question why the animals became overweight.

Based on previous research she had carried out in the Round lab, she suspected the microbiome was involved. She had helped demonstrate that one role of the immune system is to maintain balance among the diverse array of bacteria in the gut. Impairing the body's defences can cause certain bacterial species to dominate over others. Sometimes, the shift negatively impacts health.

Following a similar logic, Petersen and colleagues determined that the obesity observed in immune-compromised mice stemmed from the failure of the body's defence system to appropriately recognize bacteria. These mice produced fewer of the antibodies that ordinarily latch onto the microbiome like target-seeking missiles. This change made the gut less hospitable for Clostridia, leading to more fat absorption and excessive weight gain. Over time, the mice also developed signs of type 2 diabetes.

Round points out that research by others have shown that people who are obese similarly lack Clostridia, mirroring the situation in these mice. There are also some indications that people who are obese or have type 2 diabetes may have a suboptimal immune response. The hope is that understanding these connections will provide new insights into preventing and treating these pervasive health conditions.

"We've stumbled onto a relatively unexplored aspect of type 2 diabetes and obesity," said Round. "This work will open new investigations on how the immune response regulates the microbiome and metabolic disease."

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