Impact of glucagon response on early postprandial glucose excursions irrespective of residual β‐cell function in type 1 diabetes: A cross‐sectional study using a mixed meal tolerance test

Abstract

Aims/Introduction Controlling postprandial glucose levels in patients with type 1 diabetes (T1D) is challenging even under the adequate treatment of insulin injection. Recent studies revealed the dysregulated glucagon secretion exacerbates hyperglycemia in type 2 diabetes (T2D), but little is known in T1D. We investigated whether the glucagon response to a meal ingestion could influence the postprandial glucose excursion in patients with T1D. Materials and Methods We enrolled 34 patients with T1D and 23 patients with T2D as controls. All patients underwent a liquid mixed‐meal tolerance test. We measured levels of plasma glucose, C‐peptide, and glucagon at fasting (0 minute), 30, 60 and 120 minutes after meal ingestion. All T1D patients received their usual basal insulin and two‐thirds of the necessary dose of the premeal bolus insulin. Results The levels of plasma glucagon were elevated and peaked 30 minutes after the mixed‐meal ingestion in both T1D and T2D. The glucagon increments from fasting to each time point (30, 60 and 120 minutes) in T1D were comparable to those in T2D. Among the T1D patients, the glucagon response showed no differences between the subgroups based on diabetes duration (<5 vs. ≥5 years) and fasting C‐peptide levels (<0.10 vs. ≥0.10 nmol/L). The changes in plasma glucose from fasting to 30 minutes were positively correlated with those in glucagon, but not C‐peptide, irrespective of diabetes duration and fasting C‐peptide levels in patients with T1D. Conclusions The dysregulated glucagon likely contributes to postprandial hyperglycemia independent of the residual β‐cell functions during the progression of T1D.