ATP-Sensitive K+ Channel Closure is not an Obligatory Step for Glucose-Induced Priming of Pancreatic B-Cell
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Exposure of the B-cell to high glucose has a priming effect so that insulin release in response to subsequent stimuli is enhanced1: the phenomenon is called “Time-Dependent Potentiation (TDP)”. For glucose-induced insulin release, closure of the ATP-sensitive K+ (K+ATP) channel is an obligatory step because all of the response is eliminated by the presence of diazoxide, an opener of the channel. However, we2 and others3 found that there is a K+ATP channel-independent branch of glucose-induced signaling in the B-cell, which is dependent on elevation of cytosolic Ca2+. Here, we show that “glucose-induced priming of the B-cell” and “glucose-induced insulin release by the B-cell” are mechanistically distinct from each other: closure of K+ATP channel is a pre-requisite for the latter but not for the former. Differential effects of lowering ambient Ca2+ concentration on glucose-induced TDP4,5 and glucose-induced insulin release were also evaluated.
KeywordsInsulin Release Initial Incubation Channel Closure Priming Period Subsequent Stimulus
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- 5.Malaisse, W. J., and Sener, A., 1987 Interaction between D-glucose and Ca2+ in the priming of the pancreatic B-cell, Diabet. Res. 4: 5–8.Google Scholar