JCC: Reduced fatty acid saturation in intestinal membrane fat cells leads to chronic inflammation of CDs

Background and Objectives: The purpose of this study is to explore the metabolic spectrum of intestinal membrane fat cells and the correlation between key metabolic changes and local inflammation in the context of CDmethod: The researchers analyzed the metabolites of metabolic biopsies and intestinal membrane fat tissue biopsies and primary intestinal membrane fat cells, which were regulated by fatty acid desaturation enzyme 2 (FADS2), and primary intestinal membrane fat cells were isolated from surgical specimens from CD patients and control groupsFadS2 was expressed in vitro and in vivo using slow virus vectors and adenoviruses (AAVs), respectivelyThe interaction between intestinal membrane fat cells and inflammatory response seiswas was assessed by establishing animal models of the co-culture system and FADS2-AAV treatment3T3-L1 cells are used to clarify the potential mechanism of FADS2 loss of controlresults: The researchers observed significant changes in the levels of metabolites involved in long-chain polyunsaturated fatty acids (PUFAs) multi-step alysisGas chromatography analysis showed impaired desaturation flux to n-6 and n-3 pathways, which was associated with a decrease in FADS2 activity in human intestinal membrane tissueReduced FADS2 expression at mRNA and protein levels was shown in surgical specimensThe recovery of FADS2 expression allows the endogenousity of n-3 fatty acids to be converted into decomposable lipid media, leading to a significant reduction in inflammatory macrophage immersion and a decrease in the expression of inflammatory cytokines or fatty factorsconclusion: Reduced fatty acid saturation and lipid-mediated imbalance in the fat tissue of the intestinal membrane lead to chronic inflammation of CDThe therapeutic effects of FADS2 may lead to improved CD therapy