The effect of preceding glucose decline rate on low‐dose glucagon efficacy in individuals with type 1 diabetes: A randomized crossover trial

• Published in: Diabetes, obesity & metabolism Vol. 23; no. 4; pp. 1057 - 1062
• Main Authors: Laugesen, Christian, Schmidt, Signe, Holst, Jens Juul, Nørgaard, Kirsten, Ranjan, Ajenthen G.
• Format: Journal Article
• Language: English
• Published: Oxford, UK Blackwell Publishing Ltd 01-04-2021; Wiley Subscription Services, Inc
• Subjects: Diabetes; Diabetes mellitus (insulin dependent); Glucagon; Glucose; Glucose monitoring; hypoglycaemia; Hypoglycemia; Insulin; Pharmacodynamics; Plasma; type 1 diabetes; glucagon; type 1 diabetes; hypoglycaemia; pharmacodynamics
• ISSN: 1462-8902; 1463-1326
• DOI: 10.1111/dom.14301

Identifying determinants of low‐dose glucagon efficacy is important to optimise its utilization for prevention and treatment of hypoglycaemia in individuals with type 1 diabetes. The study objective was to investigate whether the preceding glucose decline rate affects glucose response to low‐dose glucagon administration. Ten adults with insulin pump‐treated type 1 diabetes were included in this randomized, single‐blind, two‐way crossover study. Using a hyperinsulinaemic clamp technique, plasma glucose levels were reduced with either a rapid or slow decline rate while maintaining fixed insulin levels. When the plasma glucose level reached 3.9 mmoL/L, insulin and glucose infusions were discontinued and 150 μg subcutaneous glucagon was administered, followed by 120 minutes of plasma glucose monitoring. The positive incremental area under the glucose curve after administration of low‐dose glucagon did not differ between the rapid‐decline and slow‐decline visits (mean ± SEM: 220 ± 49 vs. 174 ± 31 mmoL/L x min; P = 0.21). Similarly, no differences in total area under the glucose curve, peak plasma glucose, incremental peak plasma glucose, time‐to‐peak plasma glucose or end plasma glucose were observed. Thus, preceding glucose decline rate did not significantly affect the glucose response to low‐dose glucagon.