FIG 6.

OPN decreased the adhesion of probiotic bacteria to intestinal epithelial cells treated with high fat. (A) The relative expression of OPN in HT-29 cells that were cultured with or without 200 μmol/L of palmitic acid (PA). (B) The representative images of Lactobacillus cultured with the OPN neutralizing antibody or with recombinant OPN in the medium containing PA or not. Scale bars, 50 μm. (C) The ratio of 16S and 18S, as well as (D) the relative expression of E-cadherin and integrin β were detected in the medium containing PA or not. When blocking integrin α4, the αv chain, and OPN, (E) the levels of E-cadherin and integrin β, as well as (F) the activation of Notch signaling were detected in the supernatant containing PA. (G) The activation of Notch1 or the expression of E-cadherin was measured after the administration of OPN with or without DAPT. Experiments were conducted in triplicate. (H) OPN facilitated the metabolism of fatty acids and HFD-induced metabolic disorders by regulating the composition of gut microbiota, including Lactobacillus, and their adhesion to the intestine via the adhesion molecules E-cadherin and the Notch signaling pathway. Data are given as the mean ± SEM. A Student’s t test (panel A) and a two-way ANOVA (panels C–E and G) were used to analyze the data with n = 4 in 3 experiments. *, P < 0.05; **, P < 0.01; ***, P < 0.001.