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 AOM/DSS-induced mice. Meanwhile, the gut microbiota were disturbed, consequently fostering the metabolism of secondary bile acids. The contents of lithocholic acid (LCA) and deoxycholic acid (DCA) 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 validate 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.

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 AMPK/SIRT1 signaling through LPS.

It has been widely accepted that resistant starch (RS) provides numerous health benefits for human. In this research, we aimed at evaluating the performance of novel starch-lipid complexes, RS5, in comparison with RS2 on physical features, glucolipids metabolism, inflammation, and gut microbiota profiles of Type 2 diabetes mellitus (T2DM) rats. The T2DM model was established by streptozotocin injection to the high-fat-sugar fed rats. According to a serial of biochemical analyses, we found that RS5 diets were strongly correlated with enhanced homeostatic model assessment for insulin secretion (HOMA-IS), high-density lipoprotein cholesterol (HDL-C), adiponectin (ADP), insulin action index (IAI), glucagon-like peptide-1 (GLP1), and short-chain fatty acids (SCFAs) in T2DM rats whilst negatively associated with the low-density lipoprotein (LDL-C) and inflammatory cytokines, showing the capabilities to ameliorate T2DM symptoms by regulation of glucolipid metabolism, gut metabolites, and inflammation. On the other hand, RS2-enriched supplementations were influential in the mediation of insulin secretion to improve glucose metabolism. The increasing evidence collected herein suggested that intestinal microbiota could mediate glucolipids metabolism and alleviate inflammation after certain microflora nourished by RS. In addition, RS intake made an impact on PI3K/AKT signaling pathway that might contribute to the improvement of glucose metabolism, insulin resistance, and inflammatory responses.

D-Psicose, as a low-calorie rare sugar, has attracted a lot of attention in recent years for alternating to sucrose. The anti-obesity effect of D-psicose has been extensively confirmed in previous studies, however, the impact of D-psicose on colitis remains vague. Here, we firstly evaluated the effect of the D-psicose prophylactic intervention on dextran sulfate sodium-induced colitis in C57BL/6 mice. The pathological symptoms, inflammatory cytokines levels, gut microbiota composition, short chain fatty acids (SCFAs) production and colonic barrier integrity were comprehensively evaluated. The results confirmed that D-psicose intervention aggravated colitis, characterized by the exacerbation of colon shortening, increase of colonic inflammatory infiltration, and marked exaltation of disease activity indices and IL-6, IL-1β and TNF-α levels. Further, the dysfunction of gut microbiota was identified in the psicose group. The abundance of pro-inflammatory bacteria Lachnospiraceae_NK4A136_group was significantly up-regulated while the abundance of probiotics Akkermansia and Lactobacillus were significantly down-regulated in the psicose group compared to the model group. Moreover, the production of SCFAs was suppressed in the psicose group, accompanied by a decrease in the level of mucin 2 (Muc-2). Collectively, the underlying mechanism of the exacerbation of colitis by D-psicose intervention might be attributed to microbiota dysfunction accompanied by the reduction of SCFAs, which leads to the damage of the mucosal barrier and the intensification of inflammatory invasion.

Peanut allergy is considered to be a major health issue with global effects. To date, no effective curative approach has been applied for the therapy of the anaphylaxis resulting from the peanut allergens. The accurate and effective detection methods for the surveillance of allergens in food are still the primary strategies to avoid allergic diseases. In this study, nanobodies (Nbs) derived from the Heavy-Chain only Antibodies (HCAbs) were selected against the general peanut protein extract through the unbiased strategy to facilitate the development of the sandwich ELISA for the detection and surveillance of peanut allergen contamination. The target antigen of the selected Nb was identified as peanut allergen Ara h 3, and a cross-reaction was observed with the member of Gly 1 from the Ara h 3 family. The applicability of the self-paired Nb P43 on the establishment of the immuno-assay was verified. A sandwich ELISA against peanut allergen was developed, which reached a linear range of 0.2－10.6 μg/mL, and a limit of detection of 53.13 ng/mL.

The metabolic syndrome (MS) has become one of the main problems in public health. Tea polyphenols (TPs), the main bioactive components of tea, has been claimed to have the potential to regulate metabolism and effectively prevent or mitigate the MS. However, many studies into the effects of TPs on MS have provided conflicting findings and the underlying mechanism has been elusive. The predominant TPs in unfermentedand and fermented tea are catechins and oxidized polyphenols (theaflavins and thearubigins), both of which have low bioavailability and reach the colon where most gut microbes inhabit. Gut microbiota has been demonstrated to be tightly associated with host metabolism. The interactions between TPs and gut microbiota will lead to the alterations of gut microbiota composition and the production of metabolites including short chain fatty acids, bile acids, amino acids and TPs derived metabolites, accordingly exerting their biological effects both locally and systemically. This review highlighted the contribution of metabolites and specific gut bacteria in the process of TPs intervention on the MS and further discuss how TPs impact the MS via gut microbiota from the viewpoint of gut organ/tissue axis.