OBJECTIVES: This aim of this study is to investigate the regulation of serum uric acid (SUA) levels with canagliflozin in relation to diabetic parameters. MATERIALS AND METHODS: Drug-naïve subjects with type 2 diabetes (T2DM) received 50 - 100 mg/day canagliflozin monotherapy (n = 40) for 3 months. Levels of SUA and some diabetic parameters were monitored. RESULTS: In the overall subjects, significant negative correlations were observed between the changes (Δ) of SUA and the baseline SUA levels (R = -0.392, p < 0.02). The subjects were divided into two subgroups (n = 20 each) according to the changes of SUA levels (above the median (group A): from 4.79 ± 1.22 to 5.34 ± 1.39 mg/dL; and below the median (group B): from 5.80 ± 1.08 to 4.98 ± 0.97 mg/dL). Significant increases of SUA levels were observed in group A (11.4%, p < 0.0002), while significant decreases of SUA levels were seen in group B (-14.1%, p < 0.00001). Significant correlations were seen between the baseline levels of SUA and those of homeostasis model assessment (HOMA)-B (R = 0.463, p < 0.04) and between the changes of SUA and those of HOMA-B (R = 0.420, p < 0.05) only in group A. Higher degrees of elevations of HOMA-B and decreases of HbA1c/fasting blood glucose (FBG) were seen in group A versus group B. CONCLUSION: These results suggest that 1) high SUA levels decreased while low SUA levels increased with canagliflozin; 2) better glycemic efficacies and higher degrees of enhancement of β-cell function were observed in those with elevated SUA levels with canagliflozin; 3) SUA might be linked to modulation of β-cell function.
OBJECTIVES: This aim of this study is to investigate the regulation of serum uric acid (SUA) levels with canagliflozin in relation to diabetic parameters. MATERIALS AND METHODS: Drug-naïve subjects with type 2 diabetes (T2DM) received 50 - 100 mg/day canagliflozin monotherapy (n = 40) for 3 months. Levels of SUA and some diabetic parameters were monitored. RESULTS: In the overall subjects, significant negative correlations were observed between the changes (Δ) of SUA and the baseline SUA levels (R = -0.392, p < 0.02). The subjects were divided into two subgroups (n = 20 each) according to the changes of SUA levels (above the median (group A): from 4.79 ± 1.22 to 5.34 ± 1.39 mg/dL; and below the median (group B): from 5.80 ± 1.08 to 4.98 ± 0.97 mg/dL). Significant increases of SUA levels were observed in group A (11.4%, p < 0.0002), while significant decreases of SUA levels were seen in group B (-14.1%, p < 0.00001). Significant correlations were seen between the baseline levels of SUA and those of homeostasis model assessment (HOMA)-B (R = 0.463, p < 0.04) and between the changes of SUA and those of HOMA-B (R = 0.420, p < 0.05) only in group A. Higher degrees of elevations of HOMA-B and decreases of HbA1c/fasting blood glucose (FBG) were seen in group A versus group B. CONCLUSION: These results suggest that 1) high SUA levels decreased while low SUA levels increased with canagliflozin; 2) better glycemic efficacies and higher degrees of enhancement of β-cell function were observed in those with elevated SUA levels with canagliflozin; 3) SUA might be linked to modulation of β-cell function.