Glucagon secretion and its association with glycaemic control and ketogenesis during sodium‐glucose cotransporter 2 inhibition by ipragliflozin in people with type 1 diabetes: Results from the multicentre, open‐label, prospective study
Authors' conclusion
Ipragliflozin treatment for T1D increased postprandial glucagon secretion, which did not exacerbate postprandial hyperglycaemia but might protect against hypoglycaemia, leading to reduced glycaemic variability. The increased glucagon secretion might accelerate ketogenesis when adequate insulin is not supplied.
Study context
- Population
- Adults with T1D
- Participants
- 25 adults
- Exposure
- Before vs 12 weeks after ipragliflozin as adjunct to insulin
- Ipragliflozinn = 25
- Outcome
- Glucagon responses and their associations with glycaemic control and ketogenesis (MMTT before and after ipragliflozin)
- Follow-up
- 12 weeks
Methodological detailsmulticentre, open-label
- Multicentre
- Open-label
Main finding
As reported in the abstract
Glucagon AUC0-120min during MMTT · 12 weeks vs baseline
Glucagon AUC0-120min significantly increased in second vs first mixed-meal tolerance test (MMTT)
14%
Observational data: associations, not effects.
Further findings
- Fasting and postprandial β-hydroxybutyrate significantly elevated in second vs first MMTT
- % changes in glucagon (fasting and AUC0-120min) from baseline to 12 weeks significantly correlated with those in β-hydroxybutyrate
Original publication
Glucagon secretion and its association with glycaemic control and ketogenesis during sodium‐glucose cotransporter 2 inhibition by ipragliflozin in people with type 1 diabetes: Results from the multicentre, open‐label, prospective study. Diabetes Obes Metab. Published 22 January 2024. doi:10.
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