Researchers at Jiangnan University report that the gut bacterium Bacteroides vulgatus and one of its metabolites increased GLP‑1 secretion in mice, which led to higher FGF21 levels, improved blood sugar control and reduced sugar-seeking behavior. Mouse studies also showed that loss of the host receptor FFAR4 reduced B. vulgatus and FGF21. In a small human blood analysis (60 type 2 diabetes patients, 24 controls), FFAR4 variants linked to lower FGF21 correlated with stronger sweet preference. The findings point to a microbiome‑host hormone axis that could inform future diabetes-prevention strategies, but human trials are required.
Gut Microbe and Its Metabolite May Trigger an Ozempic‑Like GLP‑1 Response — A Potential Natural Way to Curb Sugar Cravings
Researchers at Jiangnan University report that the gut bacterium Bacteroides vulgatus and one of its metabolites increased GLP‑1 secretion in mice, which led to higher FGF21 levels, improved blood sugar control and reduced sugar-seeking behavior. Mouse studies also showed that loss of the host receptor FFAR4 reduced B. vulgatus and FGF21. In a small human blood analysis (60 type 2 diabetes patients, 24 controls), FFAR4 variants linked to lower FGF21 correlated with stronger sweet preference. The findings point to a microbiome‑host hormone axis that could inform future diabetes-prevention strategies, but human trials are required.

Gut microbe and its metabolite boost GLP‑1 and may reduce sugar cravings
Researchers report that a naturally occurring gut bacterium, Bacteroides vulgatus, and one of its digestion-derived metabolites can increase secretion of glucagon-like peptide‑1 (GLP‑1) in mice — a hormonal effect similar to that produced by GLP‑1 receptor agonist drugs such as semaglutide (Ozempic).
The team led by Jiangnan University (China) combined mouse experiments with human blood analysis to explore how gut microbes, host genes and metabolites interact to influence blood glucose control and sweet preference. Their study was published in Nature Microbiology.
Key findings
- In diabetic mice, raising levels of B. vulgatus or administering a specific metabolite produced by this species increased GLP‑1 secretion. That GLP‑1 rise was followed by higher fibroblast growth factor 21 (FGF21) levels, improved glycaemic control and reduced sugar-seeking behaviour.
- Loss of the gut receptor/gene FFAR4 in mice led to a reduction in B. vulgatus abundance and a consequent drop in FGF21 secretion, linking host genetics, microbiome composition and hormone signalling.
- In a blood analysis of 60 people with type 2 diabetes and 24 healthy controls, the researchers report that variants in FFAR4 associated with lower FGF21 were correlated with stronger reported preference for sweet foods. The human data are associative and based on a modest sample.
What this means
GLP‑1 is an endogenous hormone that promotes insulin secretion after meals and increases satiety. Pharmaceutical GLP‑1 receptor agonists mimic GLP‑1 and are effective treatments for type 2 diabetes and for weight management. The new work suggests a gut‑driven pathway that stimulates the body's own GLP‑1 and downstream FGF21 production, which could — if validated in humans — offer a complementary or preventive strategy that harnesses microbiome chemistry rather than long‑term drug therapy.
Important caveats
The mouse results are robust within the experimental context, but translation to humans is not established. The human portion of the study is correlational, with a relatively small cohort, so causality and safety remain unproven. The authors themselves caution that further preclinical and clinical studies are required to determine whether boosting specific microbes or metabolites is safe, effective and practical for preventing or treating diabetes in people.
“Our findings identify a microbiome–host hormonal axis that may modulate sugar preference and glycaemic control, but human trials are needed to test therapeutic potential,” the authors wrote.
Bottom line: The study highlights a promising microbiome‑hormone link — B. vulgatus and a metabolite that can raise GLP‑1 and FGF21 in mice — but more work is needed before this becomes a human treatment or preventive strategy.
Study citation: Published in Nature Microbiology. An earlier version of this story appeared in January 2025.
