The human gut microbiome plays a pivotal role in health and disease, notably through its interaction with bile acids (BAs). BAs, synthesized in the liver, undergo transformation by the gut microbiota upon excretion into the intestine, thus influencing host metabolism. However, the potential mechanisms of dicaffeoylquinic acids (DiCQAs) from Ilex kudingcha how to modulate lipid metabolism and inflammation via gut microbiota remain unclear. The objectives of the present study were to investigate the regulating effects of DiCQAs on diabetes and the potential mechanisms of action. Two mice models were utilized to investigate the anti-diabetic effects of DiCQAs. Additionally, analysis of gut microbiota structure and functions was conducted concurrently with the examination of DiCQAs' impact on gut microbiota carrying the bile salt hydrolase (BSH) gene, as well as on the enterohepatic circulation of BAs and related signaling pathways. Our findings demonstrated that DiCQAs alleviated diabetic symptoms by modulating gut microbiota carrying the BSH gene. This modulation enhanced intestinal barrier integrity, increased enterohepatic circulation of conjugated BAs, and inhibited the farnesoid X receptor-fibroblast growth factor 15 (FGF15) signaling axis in the ileum. Consequently, the protein expression of hepatic FGFR4 fibroblast growth factor receptor 4 (FGFR4) decreased, accompanied by heightened BA synthesis, reduced hepatic BA stasis, and lowered levels of hepatic and plasma cholesterol. Furthermore, DiCQAs upregulated glucolipid metabolism-related proteins in the liver and muscle, including v-akt murine thymoma viral oncogene homolog (AKT)/glycogen synthase kinase 3-beta (GSK3β) and AMP-activated protein kinase (AMPK), thereby ameliorating hyperglycemia and mitigating inflammation through the down-regulation of the MAPK signaling pathway in the diabetic group. Our study elucidated the anti-diabetic effects and mechanism of DiCQAs from I. kudingcha, highlighting the potential of targeting gut microbiota, particularly Acetatifactor sp011959105 and Acetatifactor muris carrying the BSH gene, as a therapeutic strategy to attenuate FXR-FGF15 signaling and ameliorate diabetes.

Spermidine is a functional ingredient that can extend the lifespan of many foods and indicate meat safety. However, its synthesis and enrichment is expensive and complex. To develop an effective separation material that can offer highly selective recognition of spermidine, we first applied non-covalent molecular imprinting technology using methacrylic acid as a functional monomer, azobisisobutyronitrile as an initiator, and ethylene glycol dimethacrylate as a cross-linker. The adsorption properties of the polymers were analyzed using the Scatchard equation, the Lagergren kinetic equation, and the static distribution coefficient. The optimal polymerization molar ratio of the template molecule spermidine to the functional monomer was 1:4, the maximum adsorption amount was 97.75 μmol/g, and the adsorption equilibrium time was 300 min. The selective experiment showed that the interfering substances tyramine and histamine had selectivity factor α values of 2.01 and 1.78, respectively, indicating that the prepared polymer had good spermidine recognition ability. The density function theory calculations showed that the hydrogen bond strength, steric effect, and product energy caused adsorption and separation differences among the different imprinted polymer complexes.