Gut bacteria found to prevent obesity in mice

Rijma Khan
Decoders Society
Published in
3 min readSep 6, 2019

Clostridia is found to prevent weight gain in mice by blocking the intestine’s ability to absorb fat, pointing to possibilities for new therapies against obesity.

link between gut bacteria obesity and the immune system…..

The specific class of bacteria, called Clostridia, prevented mice with a compromised immune system from becoming obese, says the study published in the journal Science. The researchers found that one or more molecules produced by Clostridia prevented the gut from absorbing fat. The same class of bacteria is also found in the human gut, says the team. The results, according to researchers at the University of Utah Health, suggest an exciting potential for new ‘microbiome-based’ therapies for obesity and other metabolic diseases.

“They are the first to identify a class of bacteria that protect from obesity and metabolic syndrome. Moreover, they identify that the immune system is a critical aspect to controlling the microbiota to prevent obesity,”

Over the past century, obesity and metabolic syndrome have developed into a global epidemic. Currently, millions of people are obese and at risk of developing metabolic dysfunctions such as type 2 diabetes and cardiovascular and liver diseases. According to the World Health Organization (WHO), in 2016, more than 1.9 billion adults, 18 years and older, were overweight, and of these, over 650 million were obese.

The study shows that healthy mice have plenty of Clostridia, which is a class of 20 to 30 bacteria. However, those with an impaired immune system lose these microbes from their gut as they age, and even when the mice are fed a healthy diet, they inevitably become obese. Giving this class of microbes back to these animals allowed them to stay slim, says the study. The team found that Clostridia prevented weight gain by blocking the intestine’s ability to absorb fat. Mice, which were 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, shows analysis.

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 the clostridia to the immune impaired mice prevents obesity.

When questioned if the same class of bacteria that prevents mice from becoming obese can help control weight in people, Dr. Round told MEAWW, that “these same changes are observed in humans, so it is possible. They said that We need to do more work to investigate this.” The results could lead to a therapeutic approach, with advantages over the fecal transplants and probiotics that are now being investigated as ways to restore a healthy microbiota, says Dr. Round.

The researchers are planning future studies to examine how these beneficial gut bacteria can help humans. And the next step, according to the research team, is to isolate the molecules — that prevent the gut from absorbing fat — and further characterize how they work to determine whether they could lead to focused treatments for obesity, type 2 diabetes, and other related metabolic disorders.

“So these bacteria have evolved to live with us and benefit us, and we have a lot to learn from them. With this study, we have stumbled onto a relatively unexplored aspect of type 2 diabetes and obesity. This work will open new investigations on how the immune response regulates the microbiome and metabolic disease,”

In a related article in Science, researchers from The University of Texas Southwestern Medical Center at Dallas, state that the findings of the current study illustrate how immune system defects can lead to metabolic disease. “These findings should encourage further investigation of how the gut microbiota regulates metabolism in humans and could inspire the development of new strategies for treating metabolic disease by manipulating the microbiota”.

References

https://science.sciencemag.org/content/365/6451/eaat9351

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