ArticleCellular and molecular gastroenterology and hepatology2026
Disturbance of Oxylipin Metabolism Mediated by Autophagy of Mesenteric Adipocytes Orchestrates Gut Inflammation in Crohn's Disease.
Article in Cellular and molecular gastroenterology and hepatology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
BACKGROUND &
aimsHypertrophy of mesenteric adipose tissue (MAT) and formation of creeping fat (CF) is a typical hallmark of Crohn's disease (CD). MAT of CD patients exhibited disturbed oxylipin metabolism. This study aimed to explore the role of oxylipin in modulating gut inflammation and the underlying mechanism for the regulation of oxylipin metabolism.
methodsMAT biopsies were recruited from 14 patients with CD and 12 controls, and oxylipin analysis was performed. A series of in vitro and in vivo experiments were conducted to explore the effect of oxylipin and the corresponding metabolic enzymes on shaping immune cells. Western blot, quantitative polymerase chain reaction (q-PCR) and immunofluorescence were performed to further verify the underlying mechanisms.
resultsThe oxylipin assays revealed the end product derived from CYP450-epoxide hydrolase-mediated metabolic pathway was notably increased in CF. The upregulation of soluble epoxide hydrolase (sEH) contributed to the disturbance of oxylipin metabolism. Beclin-1 (BCN1) mediated autophagy of mesenteric adipocytes regulated sEH expression through p62-Keap1-Nrf2 pathway. Inhibition of BCN1 increased the downstream pro-inflammatory oxylipin concentration and promoted M1-like macrophages. The adipocyte-specific BCN1 knockout mice (Becn1
conclusionsOur findings showed that BCN1-mediated autophagy of adipocytes from MAT inhibited pro-inflammatory oxylipins via promoting sEH-related metabolic pathway, suggesting fatty acid metabolism and sEH/BCN1 as potential therapeutic targets for controlling gut inflammation in CD.
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