Effect of potassium ions on insulin release in the rat from the perifused islets of Langerhans with slow-rise glucose stimulation.

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Abstract
The role of extracellular K+ in the mechanism of glucose-induced insulin release in the rat was investigated by both dynamic and kinetic analyses of insulin release from islets of Langerhans by slow-rise glucose stimulation in the presence of 6.2 or 12.4 mM K+ or in its absence. The dose-response curves were sigmoidal in profile with a tendency to show a similar maximal rate of insulin release, but the Km values were very different. In particular, removal of K+ from the medium reduced the Km value from 8.9 mM (control) to 3.7 mM glucose. Hill''s constant (n) was reduced from 5.7 (control) to 4.2 in the absence of K+ and 4.4 in the presence of 12.4 mM K+. The Hill plots were linear with slopes of 4.2 (0 mM K+) and 5.7 (6.2 mM K+), respectively, whereas in the presence of 12.4 mM K+ the Hill plot consisted of 2 straight lines with a break at 4.7 mM glucose (n = 1.4 and 4.4). K+ in the medium play important roles not only as an electrolyte in connection with the integrity of the B cell membrane, but also as a heterotropic inhibitory effector in the allosteric interaction between the glucoreceptors, leading to a depression of insulin release at low glucose concentrations.