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Publication Name World Journal of Gastroenterology
Manuscript ID 125044
DOI 10.3748/wjg.125044
Country United States
Category Gastroenterology & Hepatology
Manuscript Type Basic Study
Article Title Lauric acid attenuates 14-day DDC-induced cholangiopathy in association with reduced NF-κB-CCL2 signaling and restored LRH-1-regulated gene expression
Manuscript Source Unsolicited Manuscript
All Author List Swati Ghosh, Michael W Devereaux, Colin C Anderson, David J Orlicky and Ronald J Sokol
Funding Agency and Grant Number
Funding Agency Grant Number
the Childhood Liver Disease Research Network (NIDDK, NIH) U01DK062453
Corresponding Author Swati Ghosh, Principal Investigator, Section of Pediatric Gastroenterology, Hepatology and Nutrition, Department of Pediatrics, University of Colorado Anschutz School of Medicine, 12700 East 19th Avenue, Aurora, CO 80045, United States. swati.ghosh@cuanschtz.edu
Key Words Lauric acid; Liver receptor homolog-1; Cholestasis; Hepatocyte; Macrophage; Nuclear factor-kappa B; 3,5-diethoxycarbonyl-1,4-dihydrocollidine
Core Tip Lauric acid (LA), a dietary medium-chain fatty acid, was studied in a 14-day 3,5-diethoxycarbonyl-1,4-dihydrocollidine-induced mouse model. Concurrent 5% LA supplementation attenuated biochemical cholestasis, hepatocellular injury, ductular reaction, collagen deposition, oxidative stress, senescence, and cell-death markers. These effects were associated with reduced nuclear factor-kappa B - C-C motif chemokine ligand 2 signaling, restored liver receptor homolog-1-regulated gene expression, and increased hepatic dilauroylphosphatidylcholine abundance. This study demonstrates a decrease in the development of liver injury but was not designed to demonstrate reversal of established liver injury. Further investigation will be needed to determine if liver receptor homolog-1 or dilauroylphosphatidylcholine is required for LA protection in this model.
Citation Ghosh S, Devereaux MW, Anderson CC, Orlicky DJ, Sokol RJ. Lauric acid attenuates 14-day DDC-induced cholangiopathy in association with reduced NF-κB-CCL2 signaling and restored LRH-1-regulated gene expression. World J Gastroenterol 2026; In press
PDF 125044-in-press.pdf
Received
2026-06-30 02:43
Peer-Review Started
2026-06-30 02:43
First Decision by Editorial Office Director
Return for Revision
2026-07-17 02:34
Revised
2026-07-30 16:40
Publication Fee Transferred
2026-08-21 15:31
Second Decision by Editor
2026-09-29 02:47
Second Decision by Editor-in-Chief
Final Decision by Editorial Office Director
2026-09-29 09:44
Articles in Press
2026-09-29 09:44
Edit the Manuscript by Language Editor
Typeset the Manuscript
ISSN 1007-9327 (print) and 2219-2840 (online)
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/
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