Oxidized triglyceride monomers are the main cytotoxic products of deep-frying oil. However, its impact on the intestinal barrier, the first health guardian, remains unknown. In this study, HPLC-MS/MS analysis revealed that the epoxy group is the main oxidation product, indicating that it may be the main cytotoxic factor. Therefore, 1-9,10-epoxystearic ester, 2,3-dioleic acid (EGT) and glycerol trioleate (GT) were used to reveal the effect of the epoxy group on the intestinal barrier of dextran sulfate sodium-induced colitis. Characteristics analysis showed that EGT could aggravate intestinal damage. The relative mRNA expression analysis suggested that EGT could activate Caspase-1/NLRP3/GSDMD, thereby inducing pyroptosis. The proinflammatory cytokines activated by pyroptosis and the cGAS-STING pathway were released through the pores, thus inducing the disintegration of the tight junction between the intestinal epithelial cells and enhancing intestinal permeability. Metabonomics further confirmed that EGT can change the composition and content of phospholipids on the cell membrane, indicating the morphological changes of the intestinal epithelial cell membrane. In conclusion, this study highlights that EGT induced intestinal dysfunction via Caspase-1/NLRP3/GSDMD and cGAS-STING pathways.

Summary Deep‐frying oil intake is considered to destroy body health. In this review, a meta‐analysis was performed to assess the effects of deep‐frying oil intake on the risk of intestinal barrier dysfunction. Following Preferred Reporting Items for Systematic Reviews and Meta‐Analyses guidelines, a systematic literature search was conducted in PubMed, Embase and Cochrane Central updated till April 2022 (CRD42022326306). A total of nine studies were included. The pooled results revealed that deep‐frying oil intake significantly exaggerated crypt damage of colon [weighted mean difference (WMD) = 4.55; 95% CI: 2.87, 6.24, P < 0.05], increased proinflammatory cytokine expression in plasma and colon tissue, and enhanced intestinal permeability [lipopolysaccharides content (WMD: 10.11 μg mL−1, 95% CI: 7.44, 12.79 μg mL−1, P < 0.05)]. Moreover, deep‐frying oil intake could change the gut microbiota and decrease the content of microbiota‐derived short‐chain fatty acids. In conclusion, our findings provide insights into the effect of deep‐frying oil intake on the intestinal barrier dysfunction.