1088-P: Postprandial Dynamics of Glucagon Secretion in Type 2 Diabetic Patients: Changes Associated with Short-Term Improvements in Glycemic Control

Abstract

Objective: Type 2 diabetic patients were examined for their postprandial dynamics of glucagon secretion as well as for changes in these dynamics associated with short-term improvements in their glycemic control. Methods: A total of 75 type 2 diabetic patients admitted for glycemic control who were not receiving incretin-related drugs (I) and SGLT2 inhibitors (S) at admission, 5 type 1 diabetic patients, 5 nondiabetic patients were subjected to meal tolerance tests (MTTs) during early morning fasting hours at admission. Blood samples were drawn from these patients preprandially, and 30, 60, and 120 minutes postprandially to measure their glucose, C-peptide and glucagon (Mercodia) values. Of the type 2 diabetic patients, those who improved glycemic control without both I and S (n = 10), were examined for changes in the postprandial dynamics of glucagon associated with improvements in glycemic control. Results: The AUC C-peptide values was shown to be the lowest in type 1 diabetic patients, followed by type 2 diabetic patients and nondiabetic patients, and with AUC-glucose values and AUC-glucagon values were shown to be the highest in type 1 diabetic patients, followed by type 2 diabetic patients and nondiabetic patients. Of the type 2 diabetic patients, those with BMI ≥ 25 kg/m2 and BMI < 25 kg/m2 were not significantly different in their AUC glucose, while those with BMI ≥ 25 kg/m2 had significantly larger AUC C-peptide and AUC glucagon values than those with BMI < 25 kg/m2. MTTs performed after improving glycemic control showed significantly smaller AUC glucose, significantly elevated AUC C-peptide, and significantly smaller AUC glucagon values in those improving glycemic control without both I and S after admission. Conclusions: Study results are in agreement with the conventional finding that decreased α-cell insulin action associated with decreased insulin secretion or insulin resistance leads to glucagon over-secretion secondarily. Disclosure R. Kanai: None. Y. Mori: None. R. Nishimura: Research Support; Self; Boehringer Ingelheim Pharmaceuticals, Inc. Speaker’s Bureau; Self; Abbott, AstraZeneca, Boehringer Ingelheim Pharmaceuticals, Inc., Eli Lilly Japan K.K., Medtronic, Merck & Co., Inc., Novo Nordisk Inc., Sanofi K.K., Takeda Pharmaceutical Company Limited.