Relationships of Glucose, GLP-1, and Insulin Secretion With Gastric Emptying After a 75-g Glucose Load in Type 2 Diabetes

Context The relationships of gastric emptying (GE) with the glycemic response at 120 minutes, glucagon-like peptide-1 (GLP-1), and insulin secretion following a glucose load in type 2 diabetes (T2D) are uncertain. Objective We evaluated the relationship of plasma glucose, GLP-1, and insulin secretion with GE of a 75-g oral glucose load in T2D. Design Single-center, cross-sectional, post hoc analysis. Setting Institutional research center. Participants 43 individuals with T2D age 65.6 +/- 1.1 years, hemoglobin A1c 7.2 +/- 1.0%, median duration of diabetes 5 years managed by diet and/or metformin. Intervention Participants consumed the glucose drink radiolabeled with Tc-99m-phytate colloid following an overnight fast. GE (scintigraphy), plasma glucose, GLP-1, insulin, and C-peptide were measured between 0 and 180 minutes. Main Outcome Measures The relationships of the plasma glucose at 120 minutes, plasma GLP-1, and insulin secretion (calculated by Delta insulin(0-30)/ Delta glucose(0-30) and Delta C-peptide(0-30)/Delta glucose(0-30)) with the rate of GE (scintigraphy) were evaluated. Results There were positive relationships of plasma glucose at 30 minutes (r = 0.56, P < 0.001), 60 minutes (r = 0.57, P < 0.001), and 120 minutes (r = 0.51, P < 0.001) but not at 180 minutes (r = 0.13, P = 0.38), with GE. The 120-minute plasma glucose and GE correlated weakly in multiple regression models adjusting for age, GLP-1, and insulin secretion (P = 0.04 and P = 0.06, respectively). There was no relationship of plasma GLP-1 with GE. Multiple linear regression analysis indicated that there was no significant effect of GE on insulin secretion. Conclusion In T2D, while insulin secretion is the dominant determinant of the 120-minute plasma glucose, GE also correlates. Given the relevance to interpreting the results of an oral glucose tolerance test, this relationship should be evaluated further. There appears to be no direct effect of GE on either GLP-1 or insulin secretion.