AccScience Publishing / JCTR / Online First / DOI: 10.36922/JCTR026090015
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ORIGINAL ARTICLE

Influence of ursodeoxycholic acid on hepatic lipid deposition, blood glucose, and insulin levels in high-fat -fed Sprague–Dawley rats

Xiuping Bai1* ,  Yufeng Han1 ,  Lingyan Wei1 ,  Xiaojin Han1 ,  Feng Dong2
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1 Endocrinology Division, The Second Hospital of Shanxi Medical University, Taiyuan, Shanxi , China
2 Department of Radiation Oncology, The University of Texas Health Science Center at San Antonio, San Antonio, Texas , United States of America
JCTR, 026090015 https://doi.org/10.36922/JCTR026090015
Received: 24 February 2026 | Revised: 24 July 2026 | Accepted: 18 August 2026 | Published online: 8 September 2026
© 2026 by the Author(s). This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution -Noncommercial 4.0 International License (CC-by the license) ( https://creativecommons.org/licenses/by-nc/4.0/ )
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Abstract

Background: Metabolic dysfunction-associated steatotic liver disease (MASLD) is becoming a growing public health concern. MASLD often coexists with abnormal glucose metabolism. Currently, there is no standard treatment for MASLD. Aim: To elucidate the influence of ursodeoxycholic acid (UDCA) on hepatic lipid deposition, blood glucose, and insulin levels in high-fat diet-induced Sprague–Dawley (SD) rats. Methods: SD rats were randomly assigned to three groups: Group A, which comprised a normal-diet control group; Group B, which comprised a high-fat-fed group; and Group C, which comprised rats treated with UDCA combined with a high-fat diet. At the end of week 4, we performed oral glucose tolerance tests, measured liver enzymes, triglyceride (TG) and total cholesterol (TC) contents, identified morphological changes of the liver, and quantified the expression of major genes in fatty acid, glucose, and bile acid metabolic pathways using real-time polymerase chain reaction. Results: In comparison to Group A, Group B had higher postprandial glucose, insulin, C-peptide, and hepatic TG and TC concentrations (all p < 0.05); metabolism-related genes were differentially expressed in Group B. In comparison to Group B, the values of these indices were all decreased in Group C (all p < 0.05); UDCA reversed the mRNA expression of metabolism-related genes in Group C (all p < 0.05). Conclusion: UDCA administration decreased hepatic lipid content, blood glucose, and insulin levels in SD rats. Relevance for patients: UDCA may be helpful in the treatment of MASLD and its related comorbidities in clinical practice.

Graphical abstract
Keywords
Ursodeoxycholic acid
Metabolic dysfunction-associated steatotic liver disease
Glucose
Insulin
Gene expression
Funding
This study was supported by international Science and Technology Cooperation and Exchange Program from the Shanxi Science and Technology Department in China (202204041101008), ShanXi Science and Technology Department of China (201901D111378 and 2014011044-3), Department of Resource and Social Security of Shanxi Province in China (2016–97), ShanXi Scholarship Council of China (2014–078), Merck Diabetes Research Program of Chinese Medical Association (13061040489).
Conflict of interest
The authors declare they have no competing interests.
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Journal of Clinical and Translational Research, Electronic ISSN: 2424-810X Print ISSN: 2382-6533, Published by AccScience Publishing
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