Gao T, Zhong KP, Wang JZ, Chen Y, Li CX. Allyl isothiocyanate ameliorates metabolic dysfunction-associated steatotic liver disease via vitamin D receptors in hepatocytes. World J Gastroenterol 2026; 32(4): 113647 [DOI: 10.3748/wjg.v32.i4.113647]
Corresponding Author of This Article
Chun-Xiao Li, PhD, Doctor, Department of Gastroenterology, The First Affiliated Hospital of Ningbo University, No. 59 Liuting Street, Haishu District, Ningbo 315010, Zhejiang Province, China. 11418130@zju.edu.cn
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Gastroenterology & Hepatology
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Basic Study
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This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/
Jan 28, 2026 (publication date) through Jan 23, 2026
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World Journal of Gastroenterology
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1007-9327
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Gao T, Zhong KP, Wang JZ, Chen Y, Li CX. Allyl isothiocyanate ameliorates metabolic dysfunction-associated steatotic liver disease via vitamin D receptors in hepatocytes. World J Gastroenterol 2026; 32(4): 113647 [DOI: 10.3748/wjg.v32.i4.113647]
World J Gastroenterol. Jan 28, 2026; 32(4): 113647 Published online Jan 28, 2026. doi: 10.3748/wjg.v32.i4.113647
Allyl isothiocyanate ameliorates metabolic dysfunction-associated steatotic liver disease via vitamin D receptors in hepatocytes
Ting Gao, Kang-Peng Zhong, Jun-Zhuo Wang, Yi Chen, Chun-Xiao Li
Ting Gao, Kang-Peng Zhong, Jun-Zhuo Wang, Chun-Xiao Li, Department of Gastroenterology, The First Affiliated Hospital of Ningbo University, Ningbo 315010, Zhejiang Province, China
Yi Chen, Department of Gastroenterology, The First Affiliated Hospital, College of Medicine, Zhejiang University, Hangzhou 310003, Zhejiang Province, China
Co-first authors: Ting Gao and Kang-Peng Zhong.
Co-corresponding authors: Yi Chen and Chun-Xiao Li.
Author contributions: Li CX and Chen Y conceived of the study; Gao T, Zhong KP, and Wang JZ performed the experiments; Gao T and Zhong KP analyzed the data and wrote the paper; Li CX revised the paper; all authors reviewed and approved the final version of the manuscript.
Supported by the Natural Science Foundation of Zhejiang Province, No. LQ22H030001; the Natural Science Foundation of Ningbo, No. 2024J474; the Ningbo Top Medical and Health Research Program, No. 2023020612; and the Project of Ningbo Leading Medical and Healthy Discipline, No. 2022-S04.
Institutional review board statement: This study did not involve human subjects or living animals.
Institutional animal care and use committee statement: This study does not involve animal research.
Conflict-of-interest statement: The authors declare that they have no conflict of interest.
Data sharing statement: The data in this study are available from the corresponding author on reasonable request.
Open Access: This article is an open-access article that was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution NonCommercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: https://creativecommons.org/Licenses/by-nc/4.0/
Corresponding author: Chun-Xiao Li, PhD, Doctor, Department of Gastroenterology, The First Affiliated Hospital of Ningbo University, No. 59 Liuting Street, Haishu District, Ningbo 315010, Zhejiang Province, China. 11418130@zju.edu.cn
Received: September 1, 2025 Revised: October 24, 2025 Accepted: November 19, 2025 Published online: January 28, 2026 Processing time: 143 Days and 18.1 Hours
Abstract
BACKGROUND
Prior studies indicate that allyl isothiocyanate (AITC) alleviates metabolic dysfunction-associated steatotic liver disease (MASLD). The vitamin D receptor (VDR) is known to exert protective effects in MASLD; however, whether AITC alleviates MASLD through VDR remains unclear.
AIM
To clarify the function and underlying mechanisms of AITC in MASLD via VDR.
METHODS
AML-12 cells were exposed to 300 μM palmitate acid (PA) for 24 hours to establish an in vitro MASLD model, followed by treatment with AITC (20 μM). We quantified intracellular lipid content using oil red O staining and biochemical triglyceride assays, and measured the expression of key regulators of hepatic de novo lipogenesis, fatty-acid (FA) β-oxidation, and insulin-resistance-related signaling by immunoblotting and quantitative real-time polymerase chain reaction.
RESULTS
To establish an in vitro MASLD model, AML-12 cells were treated with 300 μM PA for 24 hours. In this model, AITC significantly reduced protein levels associated with lipid synthesis and insulin resistance while upregulating those involved in FA β-oxidation. AITC enhanced VDR expression and increased the expression of hepatocyte nuclear factor 4 alpha (HNF-4α) and the downstream targets microsomal triglyceride transfer protein (MTTP) and apolipoprotein B (ApoB). These changes mitigated PA-induced lipid accumulation, alleviated insulin resistance, and stimulated FA β-oxidation. Additionally, vitamin D further enhanced the therapeutic effects of AITC on MASLD.
CONCLUSION
AITC provides a robust molecular basis for improving MASLD by activating hepatic VDR and driving the downstream HNF-4α/MTTP/ApoB signaling pathway. This pathway reduces hepatic lipid accumulation, promotes FA β-oxidation, and improves insulin resistance, establishing AITC as a promising treatment for MASLD.
Core Tip: Metabolic dysfunction-associated steatotic liver disease (MASLD) denotes a continuum of disorders unified by hepatic steatosis and can affect approximately one quarter of the global population, reaching up to 75% among individuals with obesity. This work seeks to define the functional contribution and mechanism of allyl isothiocyanate (AITC) in mitigating MASLD via the vitamin D receptor (VDR). In an in vitro MASLD model, AITC activates VDR through hepatocyte nuclear factor 4 alpha/microsomal triglyceride transfer protein/apolipoprotein B signaling, thereby reducing lipid accumulation and insulin resistance while promoting fatty acid β-oxidation. Taken together, these results show the therapeutic promise of AITC in MASLD.
