{"id":192463,"date":"2025-12-19T22:29:10","date_gmt":"2025-12-19T22:29:10","guid":{"rendered":"https:\/\/www.newsbeep.com\/nz\/192463\/"},"modified":"2025-12-19T22:29:10","modified_gmt":"2025-12-19T22:29:10","slug":"the-gut-bacteria-that-put-the-brakes-on-weight-gain-in-mice-theu","status":"publish","type":"post","link":"https:\/\/www.newsbeep.com\/nz\/192463\/","title":{"rendered":"The gut bacteria that put the brakes on weight gain in mice \u2013 @theU"},"content":{"rendered":"

Reposted from U of U Health<\/a>.<\/p>\n

The gut microbiome is intimately linked to human health and weight. Differences in the gut microbiome\u2014the bacteria and fungi in the gut\u2014are associated with obesity and weight gain, raising the possibility that changing the microbiome could improve health. But any given person\u2019s gut contains hundreds of different microbial species, making it difficult to tell which species could help.<\/p>\n

Now, research at the University of Utah has identified a specific type of gut bacteria, called\u00a0Turicibacter,\u00a0that improves metabolic health and reduces weight gain in mice on a high-fat diet. People with obesity tend to have less\u00a0Turicibacter,\u00a0suggesting that the microbe may promote healthy weight in humans as well. The results could lead to new ways to control weight by adjusting gut bacteria.<\/p>\n

The results are published in\u00a0Cell Metabolism<\/a>.<\/p>\n

A microscopic needle in a haystack
\n\"\"<\/a>Collage of microscope images showing a rod-shaped Turicibacter (foreground), cross section of intestine, and fluorescent microscopy of more bacteria (background). Images not to scale. Image credit: Kendra Klag<\/p>\n

The researchers had known from previous work that a large group of about 100 bacteria was collectively able to prevent weight gain in mice, but finding a specific microbe that was key to weight maintenance was a laborious task. \u201cThe microbes that live in our gut don\u2019t like to live outside the gut at all,\u201d said first author\u00a0Kendra Klag<\/a>. Many are killed by the presence of oxygen and must be exclusively handled in airtight bubbles.<\/p>\n

But after years of culturing individual microbes, Klag found that a rod-shaped bacterium called\u00a0Turicibacter\u00a0could single-handedly reduce blood sugar, levels of fat in the blood and weight gain for mice on a high-fat diet.<\/p>\n

\u201cI didn\u2019t think one microbe would have such a dramatic effect\u2014I thought it would be a mix of three or four,\u201d said senior author June Round<\/a>, professor of microbiology and immunology at U of U Health. \u201cSo when [Klag] brought me the first experiment with\u00a0Turicibacter\u00a0and the mice were staying really lean, I was like, \u2018This is so amazing.\u2019 It\u2019s pretty exciting when you see those types of results.\u201d<\/p>\n

A former graduate student in the Round Lab<\/a>, Klag completed her doctorate and is now a medical student at the U\u2019s Spencer Fox Eccles School of Medicine.<\/p>\n

Turicibacter appears to promote metabolic health by producing fatty molecules that are absorbed by the small intestine. When the researchers added purified\u00a0Turicibacter\u00a0fats to a high-fat diet, they had the same weight-controlling effects as\u00a0Turicibacter\u00a0itself. They don\u2019t yet know which fatty molecules are the important part\u2014the bacterium produces thousands of different fats, in what Klag describes as a \u201clipid soup\u201d\u2014but they hope to narrow down on the most important molecules in future work for potential therapeutic use.<\/p>\n

A fatty feedback loop
\n\"\"<\/a>June Round<\/p>\n

Turicibacter\u00a0appears to improve metabolic health by affecting how the host produces a fatty molecule called ceramides, the researchers found. Ceramide levels increase on a high-fat diet, and high levels of ceramides are associated with many metabolic disorders, including type 2 diabetes and heart disease. But the fats produced by\u00a0Turicibacter\u00a0are able to keep ceramide levels low, even for mice on a high-fat diet.<\/p>\n

Turicibacter\u00a0levels are themselves affected by how much fat the host eats, the researchers discovered. The bacterium won\u2019t grow if there\u2019s too much fat in its environment, so mice fed a high-fat diet will lose\u00a0Turicibacter\u00a0from their gut microbiome unless their diet is regularly supplemented with the microbe.<\/p>\n

The results point to a complex feedback loop, in which a fatty diet inhibits\u00a0Turicibacter\u00a0and fats produced by\u00a0Turicibacter\u00a0improve how the host responds to dietary fats.<\/p>\n

Future directions<\/p>\n

Turicibacter\u2019s effects are unlikely to be unique; many different gut bacteria probably contribute to metabolic health. And results based on animal models may not apply to people. \u201cWe have improved weight gain in mice, but I have no idea if this is actually true in humans,\u201d Round said.<\/p>\n

But the researchers remain hopeful that\u00a0Turicibacter\u00a0could provide a starting point for developing treatments that promote healthy metabolism and prevent excessive weight gain.<\/p>\n

\u201cIdentifying what lipid is having this effect is going to be one of the most important future directions,\u201d Round said, \u201cboth from a scientific perspective because we want to understand how it works, and from a therapeutic standpoint. Perhaps we could use this bacterial lipid, which we know really doesn\u2019t have a lot of side effects because people have it in their guts, as a way to keep a healthy weight.\u201d<\/p>\n

\u201cWith further investigation of individual microbes, we will be able to make microbes into medicine and find bacteria that are safe to create a consortium of different bugs that people with different diseases might be lacking,\u201d Klag said.<\/p>\n

The results appeared online Nov. 6 in\u00a0Cell Metabolism\u00a0as \u201cDietary fat disrupts a commensal-host lipid network that promotes metabolic health<\/a>.\u201d Co-authors include scientists from the U\u2019s Division of Microbiology & Immunology in the Department of Pathology; Department of Nutrition and Integrative Physiology in the College of Health; and the Metabolomics Core research facility. Others are from Washington University School of Medicine and Germany\u2019s Max Planck Institute for Biology.<\/p>\n

This work was supported by the National Institutes of Health, including the National Cancer Institute, the National Institute of Diabetes and Digestive and Kidney Disorders, and the National Center for Complementary and Integrative Health, as well as the Helmsley Foundation, the Burroughs Wellcome Fund and the Keck Foundation. Content is solely the responsibility of the authors and does not necessarily represent the official views of the National Institutes of Health.<\/p>\n

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