Glucagon Secretion in Diabetics in Association with Normalization of Blood Glucose Responses Against Oral Glucose Loads Using an Artificial Beta Cell System

Abstract

It is important to elucidate the precise significance of pancreatic A cell hypersecretion in the pathogenesis of diabetes mellitus. Changes in immunoreactive glucagon (IRG) response to 100 g oral glucose challenges were therefpore studied in diabetics whose blood glucose responses and plasma immunoreactive insulin concentrations (IRI) were made to simulate those of normal subjects using the artificial beta cell system originally developed by us.
In 6 non-obese adult-onset and 4 insulin-dependent diabetics whose blood glucose responses against 100 g oral glucose loading and IRI were made to simulate those of normal subjects with the artificial beta cell, the IRG responses also simulated the response in normal subjects. However in one insulindependent diabetic with high anti-insulin binding capacity, the blood glucose response against oral glucose challenge was not normalized with the artificial beta cell and IRG was paradoxically increased.
This suggested that paradoxical rises in glucagon in response to oral glucose loading observed in diabetics may be secondary to insulin deficiency.