2006/04/01 by Juris J. Meier, Lise Kjems, Johannes D. Veldhuis +2 · 2 citations
Medicine · Biochemistry, Genetics and Molecular Biology · #Pancreatic function and diabetes #Diabetes and associated disorders #Metabolism, Diabetes, and Cancer #Postprandial #Internal medicine #Endocrinology #Glucagon #Hyperglucagonemia #Insulin #Diabetes mellitus #Type 2 diabetes #Medicine #Biology
paper · pdf · doi:10.2337/diabetes.55.04.06.db05-1449
openalex publication_date 2006/04/01 · openalex created_date 2016/06/24 · openalex updated_date 2026/08/01
Type 2 diabetes is characterized by an approximately 60% loss of beta-cell mass, a marked defect in postprandial insulin secretion, and a failure to suppress postprandial glucagon concentrations. It is possible that postprandial hyperglucagonemia in type 2 diabetes is due to impaired postprandial insulin secretion. To address this, we studied eight adult Goettingen minipigs before and after an approximately 60% reduction in beta-cell mass induced by alloxan. Pigs were studied fasting and after ingestion of a mixed meal. Insulin and glucagon secretion were determined by deconvolution of blood hormone concentrations measured at 1-min intervals. The relationship between insulin and glucagon release was analyzed using cross-correlation and forward versus reverse cross-approximate entropy. We report that glucagon and insulin were secreted in approximately 4-min pulses. Prealloxan, postprandial insulin secretion drove an approximately 20% suppression of glucagon concentrations (P < 0.01), through inhibition of glucagon pulse mass. The alloxan-induced approximately 60% deficit in beta-cell mass lead to an approximately 70% deficit in postprandial insulin secretion and loss of the postprandial insulin-driven suppression of glucagon secretion. We conclude that postprandial hyperglucagonemia in type 2 diabetes is likely due to loss of intraislet postprandial suppression of glucagon secretion by insulin.