value of 5.23 ± 0.85 μg/mL. After simulated gastrointestinal digestion, its inhibitory activity remained stable with no significant decrease. In an insulin-resistant (IR) HepG2 cell model, treatment with SFPr-PS3A effectively promoted glucose uptake and glycogen synthesis, concomitant with the upregulation of the protein expression of Akt and GLUT2.
Wang et al. (Tue,) studied this question.