168 ± 12 mg/dL], P < 0.01). However, there was no difference in IRI with the addition of vildagliptin, and the reduction in glucagon 1 and 2 h after the test meal showed only borderline significance (85.9 ± 5.2 vs. 74.0 ± 4.2 pg/mL, P = 0.05; 75.2 ± 5.2 vs. 65.7 ± 3.4 pg/mL, P = 0.07). Fig. 1 Changes in (a) glucose concentration, (b) immune-reactive
www.selleckchem.com/products/CX-6258.html insulin, and (c) glucagon in the meal tolerance test before (open circles) and 6 months after the addition of vildagliptin (closed circles). P value indicates 4SC-202 clinical trial comparison between before and after the addition of vildagliptin. The values shown as circles are means and the bars represent the standard errors Figure 2 shows changes in AUC0–2h for glucose, IRI, and glucagon. There was a significant reduction in glucose and glucagon AUCs0–2h with vildagliptin treatment compared with baseline (22.75 ± 1.03 vs. 19.76 ± 0.73 mmol/L·h [410 ± 19 vs. 356 ± 13 mg/dL·h],
selleck inhibitor P = 0.01; 161.4 ± 9.5 vs. 141.1 ± 7.0 pg/mL·h, P = 0.04, respectively). However, IRI AUC0–2h did not differ between baseline and after addition of vildagliptin (45.6 ± 7.1 vs. 44.1 ± 7.8 μU/mL, P = 0.85). Fig. 2 Changes in the area under the curve (AUC0–2h) during the meal tolerance test for (a) glucose, (b) immune-reactive insulin, and (c) glucagon before and 6 months after the addition of vildagliptin. The values shown as circles are means and the bars represent the standard errors Table 2 shows the baseline comparison of blood glucose-related parameters between two groups based on median glucose ΔAUC0–2h (1st ≤3.56 mmol/L [64 mg/dL] vs. 2nd ≥3.61 mmol/L [65 mg/dL]), and Table 3 shows the group comparison 6 months after the addition of vildagliptin. Fasting glucose and glucose AUC0–2h at baseline were significantly higher in the group showing greater improvement (2nd group glucose ΔAUC0–2h 3.61 mmol/L [65 mg/dL], Table 2). At 6 months
after the addition of vildagliptin, HOMA-IR and glucagon ΔAUCs0–2h were significantly 4-Aminobutyrate aminotransferase lower in this group, while IRI ΔAUC0–2h showed no difference (Table 3). No adverse reactions (hypoglycemia, hepatic dysfunction, gastrointestinal dysfunction, renal dysfunction, cardiac failure, skin problems) due to vildagliptin were observed among these participants. Table 2 Comparison of glucose-related parameters at baseline between glucose ΔAUC0–2h groups after the addition of vildagliptin 1st (n = 8) (≤64 mg/dL)a 2nd (n = 7) (>64 mg/dL)a P value Male, n (%) 5 (62.5) 5 (71.4) 0.71 Age (years) 59.3 ± 3.7 51.3 ± 4.1 0.17 BMI (kg/m2) 26.5 ± 0.9 27.5 (1.3) 0.53 Agents, n (%) Glimepiride 2 (25.0) 2 (28.6) Metformin 4 (50.0) 3 (42.9) HbA1c (%) 7.43 ± 0.18 7.82 ± 0.24 0.21 HOMA-IR 2.42 ± 0.50 3.06 ± 0.70 0.21 HOMA-β 46.3 ± 8.9 30.6 ± 5.9 0.18 Fasting glucose concentration (mmol/L) 7.11 ± 0.38 8.69 ± 0.