Abstract
INTRODUCTION: Sodium glucose co-transporter 2 (SGLT2) inhibitors increase urinary glucose excretion (UGE) by reducing the renal threshold for glucose excretion, which results in decreased serum glucose concentrations in patients with type 2 diabetes mellitus (T2D). However, no study to date has determined whether larger increases in UGE after SGLT2 inhibitor treatment correspond to larger reductions in glycated hemoglobin (HbA(1C)). METHODS: We enrolled participants who were newly prescribed an SGLT2 inhibitor (dapagliflozin 10 mg or ipragliflozin 50 mg, once daily) as an add-on therapy. Patients were tested for HbA(1C) and first morning spot urinary-creatinine and -glucose concentrations immediately prior to administration of the SGLT2 inhibitor and at a 12-week follow-up appointment. We investigated the relationship between increases in morning spot UGE and decreases in HbA(1C). RESULTS: A total of 101 participants with T2D were enrolled. The median age and diabetes duration were 61.0 and 12.8 years, respectively, and the median HbA(1C) was 8.10%. SGLT2 inhibitors significantly lowered the HbA(1C) level, with a median change from baseline to week 12 of -0.60% (p < 0.001). Robust increases from baseline were seen for the morning spot urinary glucose-to-creatinine ratio (UGCR), with a median change at week 12 of 47.3 mg/mg. In the correlation analysis, the ∆HbA(1C) level showed a significant positive correlation with ∆morning spot UGCR (r = 0.395, p < 0.001). In other words, a greater reduction in HbA(1C) was correlated with a smaller increase in UGE. After adjusting for confounding variables, ∆HbA(1C) was significantly associated with ∆morning spot UGCR. CONCLUSIONS: Although SGLT2 inhibitor treatment leads to a reduced HbA(1C) level by augmenting UGE, larger increases in UGE do not correlate to larger reductions in HbA(1C). This suggests that the increase in UGE might not be an indicator of the degree of reductions in blood glucose.