Variations in ATP-Sensitive K+ Channel Activity Provide Evidence for Inherent Metabolic Oscillations in Pancreatic β-Cells

1994 ◽  
Vol 205 (1) ◽  
pp. 880-885 ◽  
Author(s):  
S. Dryselius ◽  
P.E. Lund ◽  
E. Gylfe ◽  
B. Hellman
Keyword(s):  
K Channel ◽  
Channel Activity ◽  
Β Cells ◽  
Pancreatic Β Cells ◽  
Metabolic Oscillations

scholarly journals Metabolic inhibition impairs ATP-sensitive K+ channel block by sulfonylurea in pancreatic β-cells

1998 ◽  
Vol 274 (1) ◽  
pp. E38-E44 ◽  
Author(s):  
Eri Mukai ◽  
Hitoshi Ishida ◽  
Seika Kato ◽  
Yoshiyuki Tsuura ◽  
Shimpei Fujimoto ◽  
...  
Keyword(s):  
Metabolic Inhibition ◽  
K Channel ◽  
High Dose ◽  
Dependent Manner ◽  
Channel Activity ◽  
Β Cells ◽  
Pancreatic Β Cells ◽  
Patch Clamp Technique ◽  
Channel Inhibition ◽  
Dose Dependent

The effect of metabolic inhibition on the blocking of β-cell ATP-sensitive K+ channels (KATP channels) by glibenclamide was investigated using a patch-clamp technique. Inhibition of KATP channels by glibenclamide was attenuated in the cell-attached mode under metabolic inhibition induced by 2,4-dinitrophenol. Under a low concentration (0.1 μM) of ATP applied in the inside-out mode, KATP channel activity was not fully abolished, even when a high dose of glibenclamide was applied, in contrast to the dose-dependent and complete KATP channel inhibition under 10 μM ATP. On the other hand, cibenzoline, a class Ia antiarrhythmic agent, inhibits KATP channel activity in a dose-dependent manner and completely blocks it, even under metabolic inhibition. In sulfonylurea receptor (SUR1)- and inward rectifier K+ channel (Kir6.2)-expressed proteins, cibenzoline binds directly to Kir6.2, unlike glibenclamide. Thus, KATPchannel inhibition by glibenclamide is impaired under the condition of decreased intracellular ATP in pancreatic β-cells, probably because of a defect in signal transmission between SUR1 and Kir6.2 downstream of the site of sulfonylurea binding to SUR1.

cAMP-independent decrease of ATP-sensitive K+ channel activity by GLP-1 in rat pancreatic β-cells

2000 ◽  
Vol 440 (4) ◽  
pp. 566-572 ◽  
Author(s):  
Sechiko Suga ◽  
Takahiro Kanno ◽  
Yoshiji Ogawa ◽  
Teruko Takeo ◽  
Noritaka Kamimura ◽  
...  
Keyword(s):  
K Channel ◽  
Channel Activity ◽  
Β Cells ◽  
Pancreatic Β Cells

scholarly journals Intracellular Ca2+ Modulation of ATP-Sensitive K+ Channel Activity in Acetylcholine-Induced Activation of Rat Pancreatic β-Cells

Endocrinology ◽  
2002 ◽  
Vol 143 (2) ◽  
pp. 569-576 ◽  
Author(s):  
Kyoko Nakano ◽  
Sechiko Suga ◽  
Teruko Takeo ◽  
Yoshiji Ogawa ◽  
Toshihiro Suda ◽  
...  
Keyword(s):  
K Channel ◽  
Channel Activity ◽  
Β Cells ◽  
Pancreatic Β Cells

ATP Sensitivity of the ATP-Sensitive K+Channel in Intact and Permeabilized Pancreatic β-Cells

Diabetes ◽  
2006 ◽  
Vol 55 (9) ◽  
pp. 2446-2454 ◽  
Author(s):  
Andrei I. Tarasov ◽  
Christophe A.J. Girard ◽  
Frances M. Ashcroft
Keyword(s):  
K Channel ◽  
Β Cells ◽  
Pancreatic Β Cells

scholarly journals Symbiosis of Electrical and Metabolic Oscillations in Pancreatic β-Cells

2021 ◽  
Vol 12 ◽  
Author(s):  
Isabella Marinelli ◽  
Patrick A. Fletcher ◽  
Arthur S. Sherman ◽  
Leslie S. Satin ◽  
Richard Bertram
Keyword(s):  
Mathematical Modeling ◽  
Mathematical Model ◽  
Β Cells ◽  
Pancreatic Β Cells ◽  
Intracellular Ca ◽  
Metabolic Oscillations ◽  
Insulin Exocytosis ◽  
The Relationship ◽  
Contradictory Data ◽  
Oscillatory Processes

Insulin is secreted in a pulsatile pattern, with important physiological ramifications. In pancreatic β-cells, which are the cells that synthesize insulin, insulin exocytosis is elicited by pulses of elevated intracellular Ca2+ initiated by bursts of electrical activity. In parallel with these electrical and Ca2+ oscillations are oscillations in metabolism, and the periods of all of these oscillatory processes are similar. A key question that remains unresolved is whether the electrical oscillations are responsible for the metabolic oscillations via the effects of Ca2+, or whether the metabolic oscillations are responsible for the electrical oscillations due to the effects of ATP on ATP-sensitive ion channels? Mathematical modeling is a useful tool for addressing this and related questions as modeling can aid in the design of well-focused experiments that can test the predictions of particular models and subsequently be used to improve the models in an iterative fashion. In this article, we discuss a recent mathematical model, the Integrated Oscillator Model (IOM), that was the product of many years of development. We use the model to demonstrate that the relationship between calcium and metabolism in beta cells is symbiotic: in some contexts, the electrical oscillations drive the metabolic oscillations, while in other contexts it is the opposite. We provide new insights regarding these results and illustrate that what might at first appear to be contradictory data are actually compatible when viewed holistically with the IOM.

scholarly journals Suppression of KATP channel activity protects murine pancreatic β cells against oxidative stress

2009 ◽  
Author(s):  
Belinda Gier ◽  
Peter Krippeit-Drews ◽  
Tatiana Sheiko ◽  
Lydia Aguilar-Bryan ◽  
Joseph Bryan ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Katp Channel ◽  
Channel Activity ◽  
Β Cells ◽  
Pancreatic Β Cells
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