The health benefits of teas and tea preparations in assisting with weight loss have been well documented in numerous studies. Nevertheless, there is a paucity of population-based research on the effects of consumption of tea and tea preparations on human dietary intake, gut microbial and metabolic profiles, and thus on weight loss. This study therefore focused on changes in dietary intake, gut microbiota and metabolism in healthy adults who consumed black tea for 3 consecutive weeks. Our findings showed that the consumption of black tea was associated with a notable increase in satiety prior to meals, which was observed to be more pronounced in female participants than in male participants. The consumption of black tea has been shown to increase the species richness of gut microorganisms, as evidenced by a higher number of observed operational taxonomic units (OTUs) compared the test group with the control group (203 ± 35 vs. 229 ± 18, respectively). Moreover, it improves the microbiological structure of the gut, enhances the abundance of beneficial bacteria such as Faecalibacterium and Parabacteroides, and reduces the abundance of Prevotella. Metabolomic analysis revealed 13 significantly different metabolites and 9 enriched metabolic pathways in individuals who consumed black tea. Correlation analyses of body mass index (BMI), satiety, gut flora and metabolic profiles indicate that the modulatory effects of black tea on gut flora and metabolic profiles are more effective in high BMI participant. This study may provide new insights into the relationship between black tea interventions and host satiety, gut microbiota and metabolic profiles. Furthermore, it may offer new directions and options for clinical strategies and personalized nutrition for tea and tea preparations to assist in weight loss and lipid reduction.

2-Amino-3-methylimidazo[4,5-f]quinoline (IQ) is one of mutagenic/carcinogenic heterocyclic amines (HCAs) found mainly in well-cooked meats. As a common HCAs, IQ can pose a health risk to animals as well as humans. However, to date, few studies have explored IQ's toxic effects on systemic health, and its relevant mechanism of toxicity has not been elucidated. In this study, we for the first time determined IQ accumulation and investigated the tissue damage of developing zebrafish. Zebrafish at one-month post-fertilization were exposed to IQ (80 ng/mL) for 35 days. Ultra performance liquid chromatography-tandem mass spectrometry (UPLC-MS/MS) analysis showed that IQ accumulated in multi-organ of zebrafish such as eye, spleen, gonad (ovary or testis), heart, intestine, kidney, muscle, liver, and brain. Our results showed that IQ exposure caused histopathological alterations in IQ-accumulated organs, which could compromise organ function. Exposure to IQ significantly inhibited antioxidant related indicators. Moreover, IQ exposure significantly increased mTOR gene levels. The immunohistochemical results further validated that IQ exposure tended to over activate mTOR. In addition, IQ exposure significantly reduced the expression of autophagy-related genes, and upregulated the expression of DNA damage and repair-related genes, which also detected the accumulation of fluorescence signal of DNA damage marker γ-H2AX. Furthermore, TUNEL assay showed that IQ exposure caused apoptosis. Our findings revealed that IQ could be taken up by developing zebrafish, and accumulate in multiple tissues, especially across the blood-brain barrier, accumulate in the brain, subsequently causing systemic tissue damage, urging us to pay attention to the control or intervention of IQ exposure and decreasing accumulated impairment to systemic health.

This study explores how atmospheric cold plasma (CP) modulates the nutritional and allergenic properties of Atlantic cod through structural protein alterations. CP at 10 min reduced parvalbumin content by 9.14%, likely via α-helix loss and β-sheet increase (confirmed by FTIR amide I shifts and CD analysis), which may hinder IgE epitope recognition. Antioxidant indices TAC, TFC, and TPC peaked at CP10 (21.56%, 68.48%) and CP30 (14.00%), respectively. Protein content increased by 10.76% (pre-digestion) and 30.20% (post-digestion) at CP20, while peptide release rose by 61.18% and 26.27% at CP30. Despite microstructural and conformational changes, digestibility remained stable. These findings highlight CP as a non-thermal strategy that enhances bioactive and hypoallergenic properties of cod, with potential for broader application to other high-allergen aquatic proteins.

Food allergies (FA) are characterized by Th2-dominant immune reactions and intestinal barrier dysfunction with increased incidence worldwide. Tea intake can significantly affect biological activities and health-related allergic diseases. However, the correlation between tea intake and the risk of FA or the underlying mechanism have not been well explained. This study aimed to unveil the correlation between tea intake and the risk of FA, as well as the underlying mechanisms involving gut microbiota and allergenic factors. A prospective cohort study was conducted on the connection between tea intake and the risk of FA based on the UK Biobank. A two-sample Mendelian randomization (MR) study was conducted to further analyse the causal genetic association. A murine model (BALB/c WT mice) of ovalbumin (OVA)-induced FA was utilized for experimental validation. The tea polyphenol epigallocatechin gallate (EGCG) was assessed for its effects on allergic symptoms, serum levels, Th1/Th2 cytokine balance, and gut microbiota, to elucidate the underlying mechanisms. The population study including 411,584 UK Biobank participants revealed a lowered risk of FA upon tea intake. Further analysis of MR showed no genetic association with FA incidence. The experimental analysis verified that the tea polyphenol EGCG significantly alleviated allergic symptoms, reduced OVA-specific IgE and histamine levels, and shifted the Th1/Th2 balance toward Th1 dominance. EGCG improved intestinal barrier integrity by upregulating tight junction proteins and restored the Firmicutes/Bacteroidetes ratio in the gut microbiota. Mechanistically, EGCG downregulated the TLR4/MyD88/NF-κB signalling pathway, reducing inflammation associated with allergic sensitization. A significant correlation between tea intake and FA was identified, with emphasis on EGCG-mediated intervention by mitigating symptoms, restoring immune balance, and enhancing gut health. This study provides evidence supporting the reduced risk of FA upon tea intake and unveils the mechanisms underlying tea polyphenolic EGCG-mediated underpinnings.

Methionine, an essential amino acid, is abundant in animal protein. High dietary methionine intake is associated with the promotion of colorectal cancer (CRC); however, the mechanisms remain unclear. This study aimed to investigate the underlying mechanisms of high dietary methionine promoting CRC and evaluate the effect of high dietary methionine on healthy intestine. Our results demonstrated that high dietary methionine intake exhibited a higher incidence and invasion of tumors in azoxymethane/dextran sulfate sodium-induced mice. Meanwhile, the gut microbiota were disturbed, consequently fostering the metabolism of secondary bile acids. The contents of lithocholic acid and deoxycholic acid significantly increased (P < 0.01), which further activated the bile acid membrane receptors TGR5, and then the activated TGR5 promoted tumor proliferation through STAT3 and YAP pathways. Pseudo-germ-free mice validated the role of gut microbiota and secondary bile acids in promoting CRC by high dietary methionine. Notably, similar disturbances in gut microbiota and bile acid metabolism were observed in the intestine of healthy mice with high dietary methionine intake. In conclusion, dysregulation of bile acid metabolism and activation of the corresponding receptor TGR5 were mechanisms promoting CRC associated with high dietary methionine intake.

Citrus Pu-erh (CP) tea has gained widespread popularity due to its health benefits, particularly its hypolipidemic and anti-obesity properties. However, human studies on CP tea's metabolic benefits and underlying gut microbiome mechanisms are limited. This study evaluated the impact of CP tea on metabolic health in humans and high-fat diet (HFD)-induced obese mice. In the human pilot study, three weeks of CP tea consumption significantly improved body fat distribution and restructured the gut microbiota by enhancing the relative abundance of Lachnoclostridium, and Lachnospiraceae_UCG_004. Specifically, we found that the baseline Streptococcus level is a potential biomarker predicting CP tea's efficacy in body fat regulation. In obese mice, CP tea intervention significantly improved HFD-induced weight gain, dyslipidemia, hepatic lipid accumulation, and brain impairment. Integrated 16S rRNA sequencing and untargeted metabolomics revealed profound CP tea-induced modifications in microbial composition and cecal metabolite profiles, particularly elevating L-theanine, theophylline, and norepinephrine while reducing 1-methylxanthine. These metabolites also showed a strong correlation with microbiome and metabolic outcomes. These findings suggest that CP tea offers significant metabolic health benefits by modulating gut microbiome and related metabolites, and it may help with individualized nutritional management of tea's intervention.

Enrofloxacin is the first fluoroquinolone compound to be used in food animals in China, and plays an important role in the prevention and control of livestock and aquaculture diseases. However, enrofloxacin residues in foods resulting from its irregular or excessive use can damage seriously consumer health. In this review, the sample pretreatment techniques and the latest detection methods of enrofloxacin residues in foods are described, highlighting the advantages and disadvantages of the new sample pretreatment techniques and those from the national standards. This review focuses on the achievements and trends in the development of fluorescence methods, surface enhanced Raman scattering spectroscopy, microbial methods, electrochemical analysis, immunoassay and quartz crystal microbalance for the detection of enrofloxacin in foods, in an effort to offer new technical support for the monitoring of enrofloxacin residues in foods.

Chlorogenic acid (CGA), as a polyphenol abundant in daily diet, exerted various intestinal functions. However, the material basis of its intestinal bioactivities was still unclear. Our study investigated the gastrointestinal distribution of CGA using ultra high performance liquid chromatography-tandem mass spectrum (UPLC-MS/MS) and explored the main drivers leading to different metabolic fates of the metabolites. After oral administration of 50 mg/kg bw CGA to mice, CGA and sulfated metabolites were mainly determined in small intestine. Protocatechuic acid, catechol, and 3-hydroxyphenylpropionic acid were found in copious amounts in large intestine and feces. Besides, caffeic acid existed in the entire intestine and feces. In the in vitro mice/human fecal fermentation of CGA, the production of metabolites was consistent with that in the colon, indicating that microorganisms might lead to the difference in the gastrointestinal distribution of CGA metabolites. Moreover, CGA, 3-hydroxyphenylpropionic acid, protocatechuic acid, catechol, and caffeic acid reduced proinflammatory cytokines (interleukin-6 (IL-6) and tumor necrosis factor-‍α (TNF-‍α)) and increased mucin (Muc2) and tight junction (occludin) mRNA in LPS-induced Caco-2/HT-29 MTX co-culture cells. In conclusion, the biotransformation of CGA in different gastrointestinal tracts varied significantly, and its metabolites could partially support its intestinal bioactivities.

Heat processing of food has been well validated as the trigger to generate heat-processing side product of advanced lipoxidation end products (ALEs), which potentially engenders the threat on systemic health or progression of diseases, especially the accumulated effect after long-term intake. Thus, the study was proposed to evaluate the effect of dietary ALEs on health after long-term ingestion, specifically through simulating the intake of dietary ALE in mice within 9 months to investigate the intervention effect and underlying mechanism. The unexpected observation of renal insufficiency or impairment after long-term intake of dietary ALEs indicated the negative impact on renal health, which has been verified by the pathological analysis. Further studies revealed that a high-ALEs diet disrupted the intestinal barrier, with enhanced impact after disturbing the gut microbiota to potentially lower the abundance of beneficial microbiome through producing nephrotoxic metabolites. Correlation analysis showed that the proliferation of harmful bacteria and the reduction of beneficial bacteria were strongly correlated with intestinal barrier damage and the development of renal insufficiency. Furthermore, the underlying mechanism was unveiled as that ALEs could inhibit AMPK/SIRT1 signaling to fundamentally induce renal inflammation and oxidative stress. Thus, it was revealed that long-term intake of dietary ALE could result in renal impairment, and the results emphasized the control or intervention on dietary ALE to decrease to accumulated impairment on systemic health.

Advanced lipoxidation end products (ALEs) are formed by modifying proteins with lipid oxidation products. ALEs formed in the body have been linked to diabetes and hepatic disease. However, it is not known whether ALEs formed in heat-processed foods can induce metabolic diseases. Our results indicate that dietary ALEs induce lipid accumulation in the liver of mice at an early stage and continuous feeding of ALEs induces inflammation, oxidative stress and hepatic insulin resistance. The core reason for these adverse reactions is the damage to the intestinal barrier caused by ALEs. Due to the damage to the intestinal barrier, there is an increase in lipopolysaccharides (LPS) in the liver that induces hepatic lipid accumulation by modulating hepatic lipid metabolism. Furthermore, ALEs plays a major role in the regulation of metabolic diseases by directly or indirectly inhibiting AMP activated protein kinase (AMPK)/Sirtuin 1 (SIRT1) signaling through LPS.