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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. [ABSTRACT FROM AUTHOR]

Summary: Deep‐frying oil featuring total polar compound (TPC) has been found to be unhealthy. However, little information is available regarding the impact of TPC on the lipid digestion behaviour. In this study, three typical edible oils (palm oil, PO; high oleic acid peanut oil, HOA; and high linoleic acid sunflower oil, HLA) were selected to investigate the effect of deep‐frying on the lipid digestion. Digestion behaviour was monitored by pH‐Stat method in vitro. Digestibility rate analysis showed that free fatty acids release rate of all TPC groups was the slowest among corresponding fresh oils and deep‐frying oils, indicating deep‐frying decreased lipid digestion rate. Lipid droplet analysis uncovered that deep‐frying could increase lipid particle size. Correlation analysis showed the polymers in TPC are negatively correlated with digestion rate and particle size, suggesting the digestion behaviour of deep‐frying oil is related to TPC constitution. In conclusion, this study highlights that deep‐frying weaken the lipid digestion capacity, and the multiplicity of TPC distribution which vary in terms of FAs type contribute to differences of digestion behaviour in deep‐frying oils. [ABSTRACT FROM AUTHOR]

BACKGROUND Deep‐frying oil has been found to cause inflammatory bowel disease (IBD). However, the molecular mechanism of the effect of deep‐frying palm oil on IBD still remains undetermined. RESULTS: In the present study, bioinformatics and cell biology were used to investigate the functions and signal pathway enrichments of differentially expressed genes. The bioinformatics analysis of three original microarray datasets (GSE73661, GSE75214 and GSE126124) in the NCBI‐Gene Expression Omnibus database showed 17 down‐regulated genes (logFC < 0) and 2 up‐regulated genes (logFC > 0) existed in the enteritis tissue. Meanwhile, pathway enrichment and protein–protein interaction network analysis suggested that IBD is relevant to cytotoxicity, inflammation and apoptosis. Furthermore, Caco‐2 cells were treated with the main oxidation products of deep‐frying oil‐total polar compounds (TPC) and its components (polymerized triglyceride, oxidized triglycerides and triglyceride degradation products) isolated from deep‐frying oil. The flow cytometry experiment revealed that TPC and its components could induce apoptosis, especially for oxidized triglyceride. A quantitative polymerase chain reaction analysis demonstrated that TPC and its component could induce Caco‐2 cell apoptosis through AQP8/CXCL1/TNIP3/IL‐1. CONCLUSION: The present study provides fundamental knowledge for understanding the effects of deep‐frying oils on the cytotoxic and inflammatory of Caco‐2 cells, in addition to clarifying the molecular function mechanism of deep‐frying oil in IBD. © 2021 Society of Chemical Industry. [ABSTRACT FROM AUTHOR]