The composition of the gut microbiome can be altered by an impaired immune system. This alteration results in metabolic disease which leads to obesity. Researchers deduced that certain species of gut bacteria could be preventing the gut from absorbing fat and the lack of them results in weight gain. Experiments with mice were then conducted which showed this to be the case, pointing to exciting potential future anti-obesity therapies.
Researchers at the University of Utah Health have identified the specific class of bacteria from the gut that prevents mice from becoming obese. They suggest that the same microbes may similarly control weight in people. The bacteria is called Clostridia (a class of 20 to 30 bacteria) and it’s one of the many beneficial bacteria, out of the trillions of classes of bacteria and other microorganisms, that inhabit the intestine.
The research shows that healthy mice have plenty of Clostridia but those with an impaired immune system lose these microbes from their gut as they age. Which explains why even when they are fed a healthy diet, the mice inevitably become obese. When the researchers gave this class of microbes back to these animals, it enabled them to stay slim. The research has been published in the journal Science.
Study co-senior author, June Round, Ph.D., an associate professor of pathology at the University of Utah Health, said:
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.
The discovery which led to this research in the first place was something unexpected. The researchers were studying mice that were engineered to lack a gene called MyD88. The mice started gaining a lot of weight. The gene was originally being studied for its relationship to immune function in the gut, so the research had nothing to do with obesity and metabolism.
In the end, they discovered that suppressing this gene resulted in lower production of immunoglobulin A (IgA) antibodies in the gut, so the link to immune function was found. But they were left with a new question, which was how this gut-related immune mechanism resulted in metabolic disease and obesity.
They realized that gut bacteria were playing some kind of role in modulating this interaction between immune activity and obesity. In the end, they affirmed that a microbiome-related mechanism was playing a part, so the researchers set out to discover which bacterial populations could be responsible.
The new experiments revealed that Clostridia prevents weight gain by blocking the intestine’s ability to absorb fat. Desulfovibrio bacteria, on the contrary, seemed to block the colonization of Clostridia, which means that more Desulfovibrio and less Clostridia equaled higher absorption of fats in the intestine.
The mice that had only Clostridia bacteria living in their gut were leaner with had less fat than mice that had no microbiome at all. These mice with more Clostridia also had lower levels of a gene, CD36, that regulates the body’s uptake of fatty acids, as well as an increase in the abundance of a bacterial species called Desulfovibrio.
The insights from this experiment will be used to try and develop a new therapeutic approach to treating obesity that is better than fecal transplants and probiotics. At the moment, the latter are the main treatments being widely investigated as ways to restore a healthy microbiota. However, the researchers suggest their discovery could potentially lead to a better solution because probiotics and fecal transplants are based on transferring living microbiome to the gut – something that won’t work for everyone due to differences in diet and other factors that influence which of the bacteria can survive and thrive.
For now, they know from this new study that one or more molecules produced by Clostridia prevented the gut from absorbing fat. What they are working on finding out next is how they work. Once they know that, they hope to be able to develop focused treatments for obesity, type 2 diabetes, and other related metabolic disorders.
Co-leader of the study, Charisse Petersen, Ph.D., said: “These bacteria have evolved to live with us and benefit us. We have a lot to learn from them.”
The team concluded that the obesity observed in immune-compromised mice stemmed from the failure of the body’s defense system to appropriately recognize bacteria. Furthermore, impairing the body’s defenses can cause certain bacterial species to dominate over others which can negatively impact health. These changes make the gut less hospitable for Clostridia, leading to more fat absorption and excessive weight gain. The mice also developed signs of type 2 diabetes over time.
The hope is that by understanding these connections it will provide new insights into preventing and treating pervasive health conditions. Round said:
We’ve stumbled onto a relatively unexplored aspect of type 2 diabetes and obesity. 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. This work will open new investigations on how the immune response regulates the microbiome and metabolic disease.
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