RESUMO
Food allergy is a serious public health problem, which is mainly induced by food allergens (mainly allergenic proteins). Ultrasound can change protein structure, suggesting its potential to decrease food allergenicity. The review concluded the mechanism and influence factors of ultrasound to reduce food allergenicity. The effects of ultrasound alone on some major allergenic foods such as tree nuts, shellfish, fish, egg, soy, milk, and wheat were also discussed. Moreover, ultrasound pre- and post-treatments were combined with heating, glycation, germination, hydrolysis, fermentation, irradiation and polyphenol treatment for reducing food allergenicity were also evaluated. It was found that ultrasound induced structural changes even degradation of protein to reduce the allergenicity mainly due to cavitation effects. The reduction of allergenicity through ultrasound alone was affected by ultrasound power, time, frequency and food types, while, apart from these factors, it was affected by ultrasound order and the assisted technologies conditions during ultrasound-assisted technologies. Compared to ultrasound alone treatment, the ultrasound-assisted technology exhibited high efficiency of allergenicity reduction because ultrasound treatment caused protein unfolding to accelerate allergen modification of the assisted technologies for masking and disrupting more epitopes. Thus, ultrasound treatment, especially ultrasound-assisted technologies under appropriate conditions, was promising for producing hypoallergenic foods.
RESUMO
Food allergies are a main public health disease in the world. Ultrasound is an environmentally friendly technology that typically leads to protein unfolding and loss of protein structure, which means it has the potential to be combined with other technologies to achieve a great reduction of allergenicity in foods. This review concludes the effects of the combined ultrasound with other technologies on food allergenicity from three combinations: ultrasound before other technologies, ultrasound under other technologies, and ultrasound after other technologies. Each combination affects food allergenicity through different mechanisms: (1) as for ultrasound before other technologies, ultrasound pretreatment can unfold and lose the protein structure to improve the accessibility of other technologies to epitopes; (2) as for ultrasound under other technologies, ultrasound can continuously affect the accessibility of other technologies to epitopes; (3) as for ultrasound after other technologies, ultrasound further induces structural changes to mask and disrupt the epitopes. The reduction of allergenicity is related to the ultrasound/other technologies conditions and food types/cultivars, etc. The comparison of ultrasound before, under, and after other technologies to decrease food allergenicity should be further investigated in the future. The combination of ultrasound with other technologies is promising to produce hypoallergenic foods.
Assuntos
Alérgenos , Hipersensibilidade Alimentar , Hipersensibilidade Alimentar/imunologia , Hipersensibilidade Alimentar/prevenção & controle , Humanos , Alérgenos/imunologia , Alérgenos/química , Animais , Manipulação de Alimentos/métodos , Ultrassom , Epitopos/imunologia , Epitopos/químicaRESUMO
Background: To identify key and shared insulin resistance (IR) molecular signatures across all insulin-sensitive tissues (ISTs), and their potential targeted drugs. Methods: Three datasets from Gene Expression Omnibus (GEO) were acquired, in which the ISTs (fat, muscle, and liver) were from the same individual with obese mice. Integrated bioinformatics analysis was performed to obtain the differentially expressed genes (DEGs). Weighted gene co-expression network analysis (WGCNA) was carried out to determine the "most significant trait-related genes" (MSTRGs). Enrichment analysis and PPI network were performed to find common features and novel hub genes in ISTs. The shared genes of DEGs and genes between DEGs and MSTRGs across four ISTs were identified as key IR therapeutic target. The Attie Lab diabetes database and obese rats were used to verify candidate genes. A medical drug-gene interaction network was conducted by using the Comparative Toxicogenomics Database (CTD) to find potential targeted drugs. The candidate drug was validated in Hepa1-6 cells. Results: Lipid metabolic process, mitochondrion, and oxidoreductase activity as common features were enriched from ISTs under an obese context. Thirteen shared genes (Ubd, Lbp, Hp, Arntl, Cfd, Npas2, Thrsp., Tpx2, Pkp1, Sftpd, Mthfd2, Tnfaip2, and Vnn3) of DEGs across ISTs were obtained and confirmed. Among them, Ubd was the only shared gene between DEGs and MSTRGs across four ISTs. The expression of Ubd was significantly upregulated across four ISTs in obese rats, especially in the liver. The IR Hepa1-6 cell models treated with dexamethasone (Dex), palmitic acid (PA), and 2-deoxy-D-ribose (dRib) had elevated expression of Ubd. Knockdown of Ubd increased the level of p-Akt. A lowing Ubd expression drug, promethazine (PMZ) from CTD analysis rescued the decreased p-Akt level in IR Hepa1-6 cells. Conclusion: This study revealed Ubd, a novel and shared IR molecular signature across four ISTs, as an effective biomarker and provided new insight into the mechanisms of IR. PMZ was a candidate drug for IR which increased p-Akt level and thus improved IR by targeting Ubd and downregulation of Ubd expression. Both Ubd and PMZ merit further clinical translational investigation to improve IR.