Metagenomic and metabolomic profiling of dried shrimp (Litopenaeus vannamei) prepared by a procedure traditional to the south China coastal area.

Sun-drying is a traditional process for preparing dried shrimp in coastal area of South China, but its impacts on nutrition and the formation of flavor-contributory substances in dried shrimp remain largely unknown. This study aimed to examine the effects of the production process on the microbiota and metabolites in dried shrimp. 16S rDNA amplicon sequencing was employed to identify 170 operational taxonomic units (OTUs), with Vibrio, Photobacterium, and Shewanella emerging as the primary pathogenic bacteria in shrimp samples. Lactococcus lactis was identified as the principal potential beneficial microorganism to accrue during the dried shrimp production process and found to contribute significantly to the development of desirable shrimp flavors. LC-MS-based analyses of dried shrimp sample metabolomes revealed a notable increase in compounds associated with unsaturated fatty acid biosynthesis, arachidonic acid metabolism, amino acid biosynthesis, and flavonoid and flavanol biosynthesis throughout the drying process. Subsequent exploration of the relationship between metabolites and bacterial communities highlighted the predominant coexistence of Bifidobacterium, Clostridium, and Photobacterium contributing heterocyclic compounds and metabolites of organic acids and their derivatives. Conversely, Arthrobacter and Staphylococcus were found to inhibit each other, primarily in the presence of heterocyclic compounds. This comprehensive investigation provides valuable insights into the dynamic changes in the microbiota and metabolites of dried shrimps spanning different drying periods, which we expect to contribute to enhancing production techniques and safety measures for dried shrimp processing.

Allocholic acid protects against α-naphthylisothiocyanate-induced cholestasis in mice by ameliorating disordered bile acid homeostasis.

Cholestasis is a pathological condition characterized by disruptions in bile flow, leading to the accumulation of bile acids (BAs) in hepatocytes. Allocholic acid (ACA), a unique fetal BA known for its potent choleretic effects, reappears during liver regeneration and carcinogenesis. In this research, we investigated the protective effects and underlying mechanisms of ACA against mice with cholestasis brought on by α-naphthylisothiocyanate (ANIT). To achieve this, we combined network pharmacology, targeted BA metabolomics, and molecular biology approaches. The results demonstrated that ACA treatment effectively reduced levels of serum AST, ALP, and DBIL, and ameliorated the pathological injury caused by cholestasis. Network pharmacology analysis suggested that ACA primarily regulated BA and salt transport, along with the signaling pathway associated with bile secretion, to improve cholestasis. Subsequently, we examined changes in BA metabolism using UPLC-MS/MS. The findings indicated that ACA pretreatment induced alterations in the size, distribution, and composition of the liver BA pool. Specifically, it reduced the excessive accumulation of BAs, especially cholic acid (CA), taurocholic acid (TCA), and ß-muricholic acid (ß-MCA), facilitating the restoration of BA homeostasis. Furthermore, ACA pretreatment significantly downregulated the expression of hepatic BA synthase Cyp8b1, while enhancing the expression of hepatic efflux transporter Mrp4, as well as the renal efflux transporters Mdr1 and Mrp2. These changes collectively contributed to improved BA efflux from the liver and enhanced renal elimination of BAs. In conclusion, ACA demonstrated its potential to ameliorate ANIT-induced liver damage by inhibiting BA synthesis and promoting both BA efflux and renal elimination pathways, thus, restoring BA homeostasis.