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Updated: Aug 13, 2026
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Quantification of the Immunosuppressant Tacrolimus on Dried Blood Spots Using LC-MS/MS
Published on: November 8, 2015
Hyodeoxycholic acid ameliorates tacrolimus-induced diabetes by modulating the FXR-FGF15 axis
Nan Hu1, Minyan Qian1,2, Yanru Liu1
1Department of Pharmacy, The Third Affiliated Hospital of Soochow University/The First People's Hospital of Changzhou, Changzhou, China.
Frontiers in Pharmacology
|August 12, 2026
Summary
Hyodeoxycholic acid (HDCA) ameliorates tacrolimus (TAC)-induced diabetes by regulating bile acid profiles and metabolic enzymes. This study reveals HDCA
Area of Science:
- Metabolomics
- Endocrinology
- Microbiome Research
Background:
- Tacrolimus (TAC) immunosuppression can induce diabetes mellitus (DM) linked to gut dysbiosis and altered bile acids.
- Investigating hyodeoxycholic acid (HDCA) as a potential therapeutic for TAC-induced DM is crucial.
Purpose of the Study:
- To explore the ameliorative effects and underlying mechanisms of HDCA on TAC-induced DM in rat models.
- To elucidate the role of the gut microbiota-bile acid axis in TAC-induced DM pathogenesis.
Main Methods:
- Verified the role of gut microbiota and bile acids using antibiotic-induced depletion.
- Administered HDCA to TAC-diabetic rats, assessing metabolic indices, bile acid profiles, and gene/protein expression (FXR, TGR5, GLP-1, FGF15, Cyp7a1, Cyp8b1, etc.).
Main Results:
- Antibiotic treatment worsened DM by disrupting the gut microbiota-bile acid axis.
- HDCA improved glucose tolerance and normalized bile acid profiles by modulating Cyp7a1 and Cyp8b1 expression.
- HDCA suppressed the FXR-FGF15 axis, reduced GLP-1 secretion, and decreased ileal FXR and hepatic Creb1/Ppargc1a expression.
Conclusions:
- HDCA significantly ameliorates TAC-induced DM through metabolic enzyme regulation and bile acid profile modulation.
- The protective mechanism involves inhibiting the FXR-FGF15 axis, enhancing GLP-1 secretion, and suppressing hepatic gluconeogenesis.
