Korean J Aerosp Environ Med.  1999 Mar;9(1):60-65.

Effect of Intracellular ATP on Zn2+ Blockade of KATP Channels in Pancreatic Beta Cells

• Song DK
• Bae JH
• Hong YS
• Park WK

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.

Keyword

KATP channel; Pancreatic beta cell; Zinc ion; ATP

MeSH Terms

Adenosine Triphosphate*
Cations
Cell Membrane
Electrophysiology
Fasting
Glucose
Insulin
Insulin-Secreting Cells*
Ion Channels
KATP Channels*
Potassium
Potassium Channels, Inwardly Rectifying
Adenosine Triphosphate
Cations
Glucose
Insulin
Ion Channels
KATP Channels
Potassium
Potassium Channels, Inwardly Rectifying