Abstract
In order to identify the step(s) of pancreatic intermediate glucose metabolism involved
in glibenclamide-stimulated insulin release, 2-deoxy-ghicose and iodoacetamide were
used as inhibitors.
In situ infusion of the dog pancreas was used as experimental design.
While 2-deoxy-glucose did not alter the pattern of glibenclamide-induced insulin release,
iodoacetamide at 0.5 or 5 mM concentrations had a clearly inhibitory effect. Sodium
pyruvate restored glibenclamide-induced insulin release when impaired by 0.5 mM iodoacetamide
but failed to do so when iodoacetamide was used at a 5 mM concentration.
The infusion of adenosinetriphosphate (ATP) allowed glibenclamide to cause insulin
release in normal amounts, even in the presence of 5 mM iodoacetamide.
It is suggested that ATP production resulting from pancreatic intermediate glucose
metabolism regulates glibenclamide-induced insulin secretion.
Key words
Beta Cell - Glucose Metabolism - 2-Deoxyglucose - Iodoacetamide - ATP - Glibenclamide
