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In this study, we investigated the effect of goat milk casein hydrolysates on glucose consumption rate, intracellular glycogen concentration, and mRNA expression of gluconeogenesis-related genes, including phosphoenolpyruvate carboxykinase 1 (PCK1) and glucose-6-phosphatase catalytic subunit (G6PC), in insulinresistant HepG2 cells. From the obtained hydrolysates, we also purified and characterized novel peptides that ameliorated high-glucose-induced insulin resistance in HepG2 cells. The 3-h hydrolysate caused the highest glucose consumption rate in insulin-resistant HepG2 cells. It also showed positive effects on promoting intracellular glycogenesis and reducing mRNA expression of PCK1 and G6PC. We separated the obtained hydrolysates into 3 fractions (F1, F2, and F3) by gel filtration chromatography; we further purified F1 using reversedphase HPLC and identified peptides using liquid chromatography-tandem mass spectrometry. The bioactive peptides identified were SDIPNPIGSE (α S1 -casein, f195-204), NPWDQVKR (α S2 -casein, f123-130), SLSS-SEESITH (β-casein, f30-40), and QEPVLGPVRGPFP (β-casein, f207-219). Our findings indicated that specific bioactive peptides from goat milk casein hydrolysates ameliorated insulin resistance in HepG2 cells that had been treated with high glucose. This is a first step toward determining whether goat milk casein hydrolysates can be used as food ingredients to ameliorate insulin resistance.

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Milk fat globule membrane (MFGM), which contains abundant glycoproteins and phospholipids, exerts beneficial effects on intestinal health and immunomodulation. The aim of this study was to evaluate the protective effects and possible underlying mechanisms of MFGM on cow's milk allergy (CMA) in a β-lactoglobulin (BLG)-induced allergic mice model. MFGM was supplemented to allergic mice induced by BLG at a dose of 400 mg/kg body weight. Results demonstrated that MFGM alleviated food allergy symptoms, decreased serum levels of lipopolysaccharide, pro-inflammatory cytokines, immunoglobulin (Ig) E, IgG1, and Th2 cytokines including interleukin (IL) -4, while increased serum levels of Th1 cytokines including interferon-γ and regulatory T cells (Tregs) cytokines including IL-10 and transforming growth factor-β. MFGM modulated gut microbiota and enhanced intestinal barrier of BLG-allergic mice, as evidenced by decreased relative abundance of Desulfobacterota, Rikenellaceae, Lachnospiraceae, and Desulfovibrionaceae, while increased relative abundance of Bacteroidetes, Lactobacillaceae and Muribaculaceae, and enhanced expressions of tight junction proteins including Occludin, Claudin-1 and zonula occludens-1. Furthermore, MFGM increased fecal short-chain fatty acids (SCFAs) levels, which elevated G protein-coupled receptor (GPR) 43 and GPR109A expressions. The increased expressions of GPR43 and GPR109A induced CD103 + dendritic cells accumulation and promoted Tregs differentiation in mesenteric lymph node to a certain extent. In summary, MFGM alleviated CMA in a BLG-induced allergic mice model through enhancing intestinal barrier and promoting Tregs differentiation, which may be correlated with SCFAs-mediated activation of GPRs. These findings suggest that MFGM may be useful as a promising functional ingredient against CMA.