Fig 2: Effect of treatment on (A) insulin, (B) HbA1c, (C) HOMA-IR, and (D) DPP-4. Data analyzed with one-way ANOVA, and Bonferroni’s multiple comparison test was used as a posttest to compare all pairs of columns; * indicates p < 0.05 when compared with control group, ** indicates p < 0.05 when compared with BPA-exposed group.

Fig 3: The effect of 6 weeks of treatment with vitamin D3 (10 µg/kg/day, gavage), vildagliptin (Vilda,10 mg/kg/day, gavage), or combination on metabolic syndrome (MetS)-induced changes in soleus muscle DPP-4 activity (a), serum GLP-1 (b), soleus muscle AMPK activity (c), and soleus muscle GLUT-4 (d). MetS was induced by feeding rats 3% salt and 10% fructose for 12 weeks. Values are presented as mean ± SEM (n = 6/group). One-way ANOVA, followed by Tukey’s test for multiple comparisons, was used for analysis, a vs control, b vs MetS, and.c vs vildagliptin at p < 0.05

Fig 4: The binding subsites of the various classes of dipeptidyl peptidase-4 (DPP-4) inhibitors into the DPP-4 active site (a). Docking poses of vitamin D3 or its metabolites with DPP-4 (PDB ID:2RGU) are shown, where panels b and c show 2D and 3D docking poses of cholecalciferol (green), panels d and e show 2D and 3D docking poses of calcifediol (cyan). In contrast, panels f and g show 2D and 3D docking poses of calcitriol (purple)

Fig 5: 3D binding interaction pattern of vitamin D3 (green, panel a) and calcitriol (purple, panel b) in the binding site of DPP-4 (PBD: 2RGU). The binding orientation of these compounds is similar to that of the co-crystalized inhibitor (BI 1356, linagliptin) shown in orange