Luseogliflozin Suppresses Late-Night Basal Glycemic Variability in Type 2 Diabetes: A Retrospective Observational Study.
Keishi Yamauchi
Abstract
Open AccessINTRODUCTION: Glucose fluctuations have been implicated in the development of diabetic macroangiopathy. Sodium-glucose cotransporter 2 (SGLT2) inhibitors are known not only for their glucose-lowering effects but also for their protective effects on the kidneys and heart. Basal glycemic variability (GV) during late-night periods, when external factors such as meals and physical activity are minimized, may represent a clinically important marker of intrinsic glucose regulation. However, little is known about the impact of SGLT2 inhibitors on basal GV. This study investigated the acute (within 24 hours) effect of the first administration of luseogliflozin, an SGLT2 inhibitor, on nocturnal basal GV in patients with type 2 diabetes mellitus. PATIENTS AND METHODS: Ten patients with type 2 diabetes who met the criteria were retrospectively selected. Luseogliflozin (2.5 mg/day) was initiated after baseline assessment. Continuous glucose monitoring (CGM; FreeStyle Libre Pro, Abbott Diabetes Care Inc., Alameda, California) was performed, and the coefficient of variation (CV) of glucose was calculated as an index of glycemic variability (GV). Nocturnal basal GV was evaluated between 11:00 P.M. and 3:00 A.M. on the night before and the night after the first administration. This study was retrospective because CGM data before and after luseogliflozin initiation were obtained from existing hospital records, without prior intent to evaluate this specific effect. RESULTS: CGM revealed heterogeneous nocturnal glucose patterns with small but clinically relevant fluctuations. Luseogliflozin significantly reduced nocturnal glucose CV from 11.9% ± 3.8% at baseline to 7.2% ± 4.1% after treatment (p = 0.0048). These findings indicate that even after the first dose, luseogliflozin may acutely stabilize basal glucose fluctuations during late-night periods. CONCLUSION: This is the first study to demonstrate that an SGLT2 inhibitor can suppress nocturnal basal GV immediately after initiation. Given that GV has been associated with sympathetic activation and vascular injury, these results suggest that reducing basal GV with SGLT2 inhibitors may contribute to vascular protection. Further studies with larger sample sizes and longer follow-up are warranted to confirm these observations.