Journal of Agricultural and Food Chemistry最新文献

A polyphenol-rich extract (WEAC) from coffee leaf was previously shown to protect the epithelial barrier integrity. This study investigated the protective effects of WEAC in C57BL/6 mice fed a high-fat diet (HFD). WEAC supplementation (100-200 mg/kg·bw) reduced body weight and lowered TNF-α levels in serum, colon, liver, and brain in mice. WEAC improved mouse intestinal barrier integrity by upregulating the tight-junction protein and reducing intestinal d-lactic acid leakage. Liver histology revealed reduced lipid accumulation and ballooning degeneration, corresponding to decreased triglyceride, total cholesterol, and low-density lipoprotein cholesterol levels. The WEAC intervention also decreased total bile acid levels and altered short-chain fatty acid profiles and key phytochemical metabolism. Furthermore, WEAC reduced the Firmicutes/Bacteroidetes ratio, increased the Parabacteroides, unclassified_Muribaculaceae, and Akkermansia abundance, and lowered the Blautia levels. Additionally, WEAC showed no adverse effects in mice fed a normal diet. Overall, WEAC mitigated HFD-induced intestinal barrier damage and enterohepatic function, reduced systemic inflammation, and stabilized the gut microbiome.

The rapid evolution of insecticide resistance threatens global food security, with cytochrome P450-mediated detoxification representing a key adaptive mechanism in insects. However, direct biochemical evidence linking specific P450s to pyrethroid metabolism in Plutella xylostella remains limited. Here, we investigated the molecular basis of high-level pyrethroid resistance in P. xylostella. Comparative transcriptomic analyses of a susceptible strain and two highly resistant field populations (resistance ratios >650-fold) identified PxCYP6B4 as the most strongly overexpressed P450 (>95-fold). RNA interference-mediated knockdown of PxCYP6B4 significantly increased larval susceptibility to pyrethroids, while heterologous expression in Drosophila melanogaster conferred a 5.27-fold increase in tolerance to lambda-cyhalothrin. Importantly, in vitro assays using recombinant PxCYP6B4 expressed in Sf9 cells, combined with LC-MS/MS analysis, demonstrated direct hydroxylation of lambda-cyhalothrin to 4'-hydroxy-lambda-cyhalothrin. These results establish a direct molecular and biochemical link between PxCYP6B4 overexpression and pyrethroid detoxification.

Acylation is essential in plant metabolism, protecting metabolites from enzymatic degradation, aiding xenobiotic detoxification, and regulating cellular uptake. It also enhances the stability, solubility, and bioactivity of natural products, making it valuable for drug discovery. Since HDMF (4-hydroxy-2,5-dimethyl-3(2H)-furanone; Furaneol) 6'-O-malonyl glucoside was detected in strawberries, we hypothesized that strawberry malonyltransferases (FaMATs) acylate HDMF glucoside. Genome analysis of Fragaria × ananassa and biochemical assays identified FaMAT1C, FaMAT1S, and FaMAT4C₁/S₁ as enzymes catalyzing its malonylation, producing three isomers─likely due to keto-enol tautomerism. A screening revealed the broad substrate tolerance of FaMATs, with successful malonylation observed in 67 structurally different glycosides. Notably, FaMAT4C₁/S₁ malonylated maple furanone glucoside at the 6-OH position of the glucose moiety resulted in previously unknown metabolites. This modification stabilizes glycosides by preventing glycosidic bond cleavage by glycosidases. Understanding FaMAT function deepens insights into plant specialized metabolism and supports the development of natural product-based therapeutics.

High-fat diet (HFD) is a recognized risk factor that exacerbates intestinal inflammation and complicates colitis pathology, posing challenges for treatment. This study evaluated citrus-derived exosome-like nanoparticles (CELNs) as a dietary intervention. Results demonstrated that CELNs effectively ameliorated HFD-aggravated colitis, improving the disease activity, colon length, and immune organ index. Mechanistically, CELNs restored gut barrier integrity (upregulating occludin and ZO-1), suppressed oxidative stress and pro-inflammatory signaling, and rebuilt microbial dysbiosis (enriching Faecalibaculum and Bacteroides). Furthermore, CELNs normalized critical metabolic pathways by increasing short-chain fatty acid production, reshaping bile acid profiles (increasing chenodeoxycholic acid and deoxycholic acid content), promoting anti-inflammatory indole derivatives (especially indole acrylic acid), and modulating branched-chain amino acid metabolism. This study highlights CELNs as a potent dietary intervention strategy that rectifies dysbiosis and subsequent metabolic disorders, strengthening the intestinal barrier, and suppressing inflammation. Therefore, CELNs represent a promising novel strategy for treating complex metabolic-inflammatory gut diseases.