Objective: We have shown that "euglycemic DKA" in patients with type 1 diabetes receiving a sodium-glucose cotransporter 2-inhibitor (SGLT2i) is due to normal increases in rates of ketogenesis but blunted increases in plasma glucose levels. In this analysis, we assessed whether rescue treatment of early ketoacidosis with insulin is altered by SGLT2i use.
Research design and methods: Participants received 0.2 U/kg of aspart insulin after two 6-h interruptions of basal insulin that increased beta-hydroxybutyrate (BHB) by 1.2 ± 0.7 mmol/L before and by 1.5 ± 0.2 mmol/L during canagliflozin treatment. BHB and free fatty acid (FFA) were monitored every 30 min for 120 min after receiving a 0.2 U/kg subcutaneous injection of aspart insulin.
Results: Ten adults (23 ± 5 years) were studied. During the 120 min after rescue therapy with insulin, the reductions in BHB and FFA were nearly identical between the pre- and during canagliflozin treatment studies, respectively (-1.27 ± 0.76 and -1.13 ± 0.69, P = 0.671 for BHB and -0.50 ± 0.35 vs. -0.41 ± 0.41, P = 0.603 for FFA).
Conclusion: These data indicate that turning ketogenesis off, as well as on, does not appear to be affected by SGLT2i use.
Keywords: Insulin pump.; Ketogenesis; SGLT2i; Type 1 diabetes.