Wang SR, Cao TL, Jiang HZ. From polymorphism to phenotype: FADS2 rs174538, fatty acid signatures and disease activity in Japanese Crohn’s disease. World J Gastroenterol 2026; 32(33): 117562 [DOI: 10.3748/wjg.117562]
Corresponding Author of This Article
Hui-Zhong Jiang, PhD, Professor, Researcher, Department of Gastroenterology, Dongzhimen Hospital, Beijing University of Chinese Medicine, No. 11 North Third Ring Road East, Beijing 100700, China. jianghz93@126.com
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Medicine, Research & Experimental
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editorial
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Wang SR, Cao TL, Jiang HZ. From polymorphism to phenotype: FADS2 rs174538, fatty acid signatures and disease activity in Japanese Crohn’s disease. World J Gastroenterol 2026; 32(33): 117562 [DOI: 10.3748/wjg.117562]
World J Gastroenterol. Sep 7, 2026; 32(33): 117562 Published online Sep 7, 2026. doi: 10.3748/wjg.117562
From polymorphism to phenotype: FADS2 rs174538, fatty acid signatures and disease activity in Japanese Crohn’s disease
Si-Rui Wang, Ting-Lan Cao, Hui-Zhong Jiang
Si-Rui Wang, Ting-Lan Cao, Hui-Zhong Jiang, Dongzhimen Hospital, Beijing University of Chinese Medicine, Beijing 100700, China
Author contributions: Wang SR wrote the original draft; Cao TL and Jiang HZ contributed to conceptualization, writing, reviewing and editing; Wang SR, Jiang HZ, and Cao TL participated in drafting the manuscript; and all authors have read and approved the final version of the manuscript.
Conflict-of-interest statement: All the authors report no relevant conflicts of interest for this article.
Corresponding author: Hui-Zhong Jiang, PhD, Professor, Researcher, Department of Gastroenterology, Dongzhimen Hospital, Beijing University of Chinese Medicine, No. 11 North Third Ring Road East, Beijing 100700, China. jianghz93@126.com
Received: December 10, 2025 Revised: February 14, 2026 Accepted: March 9, 2026 Published online: September 7, 2026 Processing time: 244 Days and 13.1 Hours
Abstract
Crohn’s disease (CD) arises from an interplay between genetic susceptibility, immune dysregulation, and environmental factors, including diet and lipid metabolism. Polyunsaturated fatty acids (PUFAs) and their desaturase enzymes have attracted interest because they generate inflammatory lipid mediators. Matsuzawa et al recently published a study in World Journal of Gastroenterology, examining how the FADS2 polymorphism rs174538 shapes fatty acid profiles and CD activity in a homogeneous cohort of Japanese patients. Using serum and erythrocyte membrane measures and refined δ-6 and δ-5 desaturase indices, the authors demonstrate that rs174538 is associated with lower erythrocyte delta-6 desaturase index (rd.d6di) and, strikingly, with decreased d5di and lower arachidonic acid levels, an effect that Matsuzawa et al largely attribute to tight linkage with FADS1 variants. Although rs174538 itself did not stratify CD activity, rd.d6di correlated positively with the CD Activity Index (CDAI) in rs174538 wild-type patients, suggesting that erythrocyte-based indices of desaturase activity may serve as integrative biomarkers of inflammatory burden and possibly treatment response. Limitations include modest sample size, predominantly mild disease, and no prospective dietary assessment, which temper inference and generalizability. Nonetheless, the work provides a genotype-stratified link between membrane PUFA metabolism and C-reactive protein or CDAI in CD, strengthening the case for metabolically informed biomarkers.
Core Tip: FADS variants shape polyunsaturated fatty acids (PUFAs) fatty-acid profiles, but it is uncertain whether this matters in Crohn’s disease (CD). Matsuzawa et al bring this question into a CD cohort by linking rs174538 to stable erythrocyte membrane fatty-acid patterns and desaturase indices. Notably, the relationship between an erythrocyte delta-6 desaturase index and CD Activity Index was present only in rs174538 wild-type carriers and disappeared in mutant carriers. This highlights that the same metabolic marker can carry different clinical information depending on genetic background, offering a clearer framework for interpreting lipid biomarkers and inconsistent omega-3 (n-3) PUFAs trial results in inflammatory bowel disease.
