Effect of Intracellular ATP on Zn2+ Blockade of KATP Channels in Pancreatic Beta Cells.
- Author:
Dae Kyu SONG
;
Jae Hoon BAE
;
Young Su HONG
;
Won Kyun PARK
- Publication Type:Original Article
- Keywords:
KATP channel;
Pancreatic beta cell;
Zinc ion;
ATP
- MeSH:
Adenosine Triphosphate*;
Cations;
Cell Membrane;
Electrophysiology;
Fasting;
Glucose;
Insulin;
Insulin-Secreting Cells*;
Ion Channels;
KATP Channels*;
Potassium;
Potassium Channels, Inwardly Rectifying
- From:Korean Journal of Aerospace and Environmental Medicine
1999;9(1):60-65
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
In the therapeutic or the nutritional aspects, Zn2+ has been used as a supplement in a variety of drugs. Most of divalent or trivalent cations affect ion channels in the cell membranes of various organs. In particular, Zn2+ has been regarded as a potassium (K+) channel blocker in the field of electrophysiology. ATP-sensitive K+ (KATP) channel, which is a kind of inward rectifier K+ channel, resides in the cell membrane of pancreatic beta cells and plays an important role in glucose-induced insulin secretion. The glucose increases intracellular ATP concentration, and this inhibits KATP channels. The inhibition of KATP channels activity depolarizes the cell, and subsequently, insulin is released by Ca2+ influx through the voltage- gated Ca2+ channels. Here, we demonstrate that KATP channels in the pancreatic beta cells are also the targets of extracellular Zn2+ blockade and its blockade is dependent on intracellular ATP concentration. This may be a compensatory mechanism preventing the oversecretion of insulin from the Pancreatic beta cells triggered by Zn2+ intake in a physiologically fasting condition.
