Noster research: Gut bacteria-derived molecule found to shrink fat cells and improve metabolism
KYOTO, Japan, May 14, 2025 /PRNewswire/ -- Joint study by University of Shizuoka, Kobe University, and Noster Inc. uncovers a novel postbiotic pathway for obesity prevention.
A new collaborative study from the University of Shizuoka, Kobe University, and Kyoto-based biotech company Noster Inc. has revealed that a natural compound produced by beneficial gut bacteria can directly act on fat cells, reducing their size and improving cellular metabolism. These findings, published in Nutrients, point to a new mechanism by which microbiome-derived compounds may help combat obesity and related diseases.
The compound—HYA (10-hydroxy-cis-12-octadecenoic acid)—is made when certain gut bacteria, including Lactobacillus, metabolize linoleic acid, a common dietary fat. While HYA has previously been shown to support gut health and inflammation control, this study is the first to demonstrate that it directly alters the behavior of fat cells themselves.
"We've known that metabolites from gut bacteria can influence the body, but this is the first clear evidence that HYA acts directly on adipose tissue," says Tetsuya Hosooka, Associate Professor at the University of Shizuoka and senior author of the study. "The discovery that gut bacteria can regulate fat cell function adds an exciting new dimension to our understanding of host–microbe communication."
Key findings
In the study, mice fed a high-fat diet were supplemented with HYA for five weeks. The fat cells themselves were significantly smaller compared to mice not receiving HYA—indicating a reduction in adipocyte hypertrophy, which is closely associated with insulin resistance and chronic inflammation.
The researchers then examined the effects of HYA on cultured fat cells. In these experiments, HYA-treated adipocytes accumulated less fat, showed reduced expression of fat synthesis genes (FAS, ACC1, SCD1), and increased expression of genes involved in fat oxidation (CPT1A). This shift was linked to activation of AMP-activated protein kinase (AMPK), a key energy-regulating enzyme in cells.
Importantly, the study found that HYA boosts intracellular calcium levels in fat cells, which in turn activates AMPK. This newly described mechanism is independent of GPR40 and GPR120, two receptors previously thought to mediate HYA's effects, suggesting that a different signaling route is involved.
These results reinforce the idea that postbiotics—beneficial substances produced by gut microbes—can influence metabolic health by acting directly on distant tissues.
Reference
Matsushita R, Sato K, Uchida K, Imi Y, Amano R, Kasahara N, Kitao Y, Oishi Y, Kawaai H, Tomimoto C, et al. A Gut Microbial Metabolite HYA Ameliorates Adipocyte Hypertrophy by Activating AMP-Activated Protein Kinase. Nutrients, 2025; 17(8):1393. https://doi.org/10.3390/nu17081393
Glossary
- HYA – A natural compound produced by gut bacteria from dietary fat
- Adipocyte – A cell that stores fat in the body
- AMPK – An enzyme that regulates how cells use energy
- Postbiotic – A health-promoting compound made by gut microbes
- Hypertrophy – The enlargement of individual cells, often seen in obesity
Abbreviations
AMP (adenosine monophosphate), FAS (fatty acid synthase), ACC1 (acetyl-CoA carboxylase 1), SCD1 (stearoyl-CoA desaturase 1), CPT1A (carnitine acyltransferase 1A), GPR (G protein-coupled receptor)
About Noster Inc.
Noster Inc. is a biotechnology company based in Kyoto, Japan. The company focuses on postbiotics—compounds produced by gut bacteria—to develop new approaches to healthcare. By collaborating with universities and research institutes, Noster aims to translate microbiome science into real-world solutions for chronic diseases such as obesity, diabetes, and inflammatory conditions.
CEO: Kohey Kitao
Head Office & Research Center: 35-3 Minamibiraki, Kamiueno-cho, Muko, Kyoto 617-0006, Japan
Website: https://www.noster.inc/jp/
Contact Information
Public Relations: Nanami Akatsuka
Tel: +81-75-921-5303 / Fax: +81-75-924-2702
Email: contact@noster.inc
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SOURCE Noster Inc