Fig. 5.

HYA directly regulates glucose homeostasis and GLP-1 release. Individual FAs (HYA and LA; 1 g/kg) were administered by gavage, followed by a HYA quantification in plasma (left), ileum (center), and colon (right) (n = 8 animals). b Time-course changes in plasma GLP-1 from the tail vein was measured after oral administration of FAs (n = 7 animals per group). Basal GLP-1 concentration at time 0 was set as 100%. c OGTT was analyzed 2 h after individual FA administration (HYA and LA; 1 g/kg) by gavage (n = 8 animals per group). d Individual FAs were administered, and 2 h later, time-course changes in plasma insulin from the tail vein were measured after oral administration of glucose (n = 8 animals per group). **P < 0.01; *P < 0.05 vs. control (Tukey–Kramer test). ^##P < 0.01; ^#P < 0.05 vs. HYA (Tukey–Kramer test). Results are presented as means ± SE. e STC-1 cells were treated with LA-derived gut microbial metabolites [in a dose-dependent manner (20, 100, and 200 μM)], and GLP-1 concentration was measured in culture medium (n = 6 independent cultures from three biological replicates). **P < 0.01; *P < 0.05 vs. None (Tukey–Kramer test). f LA-derived gut microbial metabolites were detected in plasma of NC-fed mice (n = 8 animals). Results are presented as means ± SE. Source data are provided as a Source Data file 5