ArticleGut microbes
Vancomycin relieves tacrolimus-induced hyperglycemia by eliminating gut bacterial beta-glucuronidase enzyme activity.
Article in Gut microbes. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 14 citations in OpenAlex.
- The gut microbiome and allograft outcomes: implications for heart transplantation.The Journal of clinical investigation · 2026Review
- Review
- Glucuronidation metabolomic fingerprinting to map host-microbe metabolism.Nature communications · 2026Article
- Pathogenic analysis of post-transplantation obesity: A comprehensive systematic review.World journal of transplantation · 2026Article
- Unraveling the mechanisms of PCOS: the interplay between gut microbiota and the immune system.Journal of ovarian research · 2026Review
- β-Glucuronidase at the Microbiota-Host Interface: Dual Regulatory Roles and Precision Modulation by Natural Products.Molecules (Basel, Switzerland) · 2026Review
- Gut microbiota-regulated unconjugated bilirubin metabolism drives renal calcium oxalate crystal deposition.Gut microbes · 2025Article
- From bench to bed: deep insights the tacrolimus-induced diabetes and gut microbiota dysbiosis.European journal of medical research · 2025Review
- Effect of Hepatic Impairment on the Pharmacokinetics of Baicalin in Rats: Critical Roles of Gut Microbiota and Hepatic Transporters.Pharmaceutics · 2025Article
- Rescuing vascular dysfunction in dorsal pancreatic arteries prevents tacrolimus-induced glucose metabolism disorder in mice.Molecular medicine (Cambridge, Mass.) · 2025Article
- Tacrolimus and diabetic rodent models.Pharmacological reports : PR · 2025Review
- Advancements in understanding the role of intestinal dysbacteriosis mediated mucosal immunity in IgA nephropathy.BMC nephrology · 2024Review
- Gut microbiota and metabolomic profile changes play critical roles in tacrolimus-induced diabetes in rats.Frontiers in cellular and infection microbiology · 2024Article
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Up to 40% of transplant recipients treated long-term with tacrolimus (TAC) develop post-transplant diabetes mellitus (PTDM). TAC is an important risk factor for PTDM, but is also essential for immunosuppression after transplantation. Long-term TAC treatment alters the gut microbiome, but the mechanisms of TAC-induced gut microbiota in the pathogenesis of PTDM are poorly characterized. Here, we showed that vancomycin, an inhibitor of bacterial beta-glucuronidase (GUS), prevents TAC-induced glucose disorder and insulin resistance in mice. Metagenomics shows that GUS-producing bacteria are predominant and flourish in the TAC-induced hyperglycemia mouse model, with upregulation of intestinal GUS activity. Targeted metabolomics analysis revealed that in the presence of high GUS activity, the hydrolysis of bile acid (BAs)-glucuronic conjugates is increased and most BAs are overproduced in the serum and liver, which, in turn, activates the ileal farnesoid X receptor (FXR) and suppresses GLP-1 secretion by L-cells. The GUS inhibitor vancomycin significantly eliminated GUS-producing bacteria and inhibited bacterial GUS activity and BAs levels, thereby enhancing L-cell GLP-1 secretion and preventing hyperglycemia. Our results propose a novel clinical strategy for inhibiting the bacterial GUS enzyme to prevent hyperglycemia without requiring withdrawal of TAC treatment. This strategy exerted its effect through the ileal bile acid-FXR-GLP-1 pathway.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.