Provera A, Sheferaw AN, Kivumbi E, Sutti S. Letter to the Editor: Xietu Hemu prescription: A novel therapeutic strategy for obesity and metabolic dysfunction-associated steatotic liver disease? World J Hepatol 2026; 18(7): 117126 [DOI: 10.4254/wjh.117126]
Corresponding Author of This Article
Salvatore Sutti, PhD, Principal Investigator, Professor, Department of Health Sciences, University of East Piedmont, Via Solaroli 17, Novara 28100, Italy. salvatore.sutti@med.uniupo.it
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Medicine, Research & Experimental
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letter
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Provera A, Sheferaw AN, Kivumbi E, Sutti S. Letter to the Editor: Xietu Hemu prescription: A novel therapeutic strategy for obesity and metabolic dysfunction-associated steatotic liver disease? World J Hepatol 2026; 18(7): 117126 [DOI: 10.4254/wjh.117126]
Alessia Provera, Anteneh Nigussie Sheferaw, Emmanuel Kivumbi, Salvatore Sutti, Department of Health Sciences, University of East Piedmont, Novara 28100, Italy
Author contributions: Provera A and Sutti S conceptualized the study; Provera A, Sheferaw AN, Kivumbi E, and Sutti S drafted the manuscript; Sheferaw AN and Kivumbi E critically revised the manuscript. All authors have read and agreed to the published version of the manuscript.
AI contribution statement: During the preparation of this manuscript, the authors used AI-based tools, specifically ChatGPT (OpenAI) and Grammarly, exclusively for language editing purposes, including grammar and spelling checks, as well as to improve clarity and readability. The manuscript, including all sections (Abstract, Introduction, Materials and Methods, Results, Discussion, and Conclusion), was entirely written by the authors, and no part of the text was generated by AI. AI tools did not contribute to the design of the study, data analysis, or interpretation of the results. Furthermore, no images or figures included in this manuscript were generated using AI. All AI-assisted outputs were carefully reviewed and validated by the authors, who take full responsibility for the content of the manuscript.
Conflict-of-interest statement: The authors report no relevant conflicts of interest for this article.
Corresponding author: Salvatore Sutti, PhD, Principal Investigator, Professor, Department of Health Sciences, University of East Piedmont, Via Solaroli 17, Novara 28100, Italy. salvatore.sutti@med.uniupo.it
Received: December 2, 2025 Revised: December 29, 2025 Accepted: January 19, 2026 Published online: July 27, 2026 Processing time: 234 Days and 11.7 Hours
Abstract
In the recent issue of the World Journal of Hepatology, Cheng et al investigated the mechanisms by which the traditional Chinese medicine Xietu Hemu prescription (XHP) exerts therapeutic effects on metabolic dysfunction-associated steatotic liver disease (MASLD). XHP has been shown to reduce hepatic lipid accumulation and improve metabolic parameters. In this study, serum containing XHP decreased lipid deposition in HepG2 cells and inhibited adipogenic differentiation of 3T3-L1 cells in a dose-dependent manner, reducing triglycerides, cholesterol, and adipogenic markers. UPLC-QTOF/MS/MS identified 233 XHP metabolites, mainly flavonoids, while network pharmacology revealed targets associated with lipid metabolism and obesity-related pathways, particularly AMPK signaling. Integrated analyses identified PPARG as a central hub gene. Functional experiments demonstrated that XHP enhances leptin secretion, activates AMPK phosphorylation, and suppresses lipogenic regulators, effects that were abolished by LEPR silencing. These findings suggest that XHP exerts anti-lipogenic effects through leptin-mediated AMPK activation, supporting its potential as a multitarget therapeutic for MASLD and related metabolic disorders.
Core Tip: The study by Cheng et al provides new insights into how Xietu Hemu prescription (XHP) may exert beneficial effects on obesity and metabolic dysfunction-associated steatotic liver disease through AMPK activation and leptin-mediated modulation of lipid metabolism. While promising, these findings should be interpreted with caution, as the specific metabolites responsible for the observed effects remain unclear, and the use of rat serum to treat human and murine cells introduces relevant translational limitations. Notably, XHP-derived metabolites may also influence inflammatory and survival pathways, including IL-17 and PI3K/AKT signaling, potentially broadening the therapeutic implications of XHP. Further studies are needed to validate these mechanisms in human systems, explore the anti-inflammatory potential of XHP, and identify its key active metabolites to enhance translational relevance.
