Effects of linoleic acid on intracellular calcium concentration in primarily cultured rat pancreatic β-cells and underlying mechanism.
- Author:
Li WANG
1
;
Rong-Guo FU
;
Xiao-Dan LIU
;
Bao-Song GUI
;
Qiang SUN
;
Chen CHEN
;
Yu-Feng ZHAO
;
Lei DONG
Author Information
1. The Second Affiliated Hospital of Medical School, Xi'an Jiao Tong University, Xi'an 710004, China.
- Publication Type:Journal Article
- MeSH:
Animals;
Calcium;
metabolism;
Insulin-Secreting Cells;
cytology;
metabolism;
Linoleic Acid;
pharmacology;
Male;
Primary Cell Culture;
Rats;
Rats, Sprague-Dawley;
Transient Receptor Potential Channels;
antagonists & inhibitors
- From:
Acta Physiologica Sinica
2010;62(6):529-534
- CountryChina
- Language:Chinese
-
Abstract:
In this study, we investigated the mechanism of linoleic acid-stimulated increase in intracellular calcium concentration ([Ca(2+)](i)) in pancreatic islet β-cells. Pancreatic islet cells were primarily isolated from rats and cultured for the experiments. The cells were loaded with Fluo-3/AM, the indicator of [Ca(2+)](i), and the intensity of Fluo-3 was measured using confocal microscope. The islet β-cells were identified by immunocytochemical staining with insulin antibody after recording. The drugs were given by perfusion system. The results showed that linoleic acid (20 μmol/L) stimulated [Ca(2+)](i) increase with the first peak increase and the following plateau increase. Linoleic acid-stimulated [Ca(2+)](i) increase was partly inhibited by removal of extracellular calcium and by transient receptor potential (TRP) channel blocker, La(3+), and it was totally blocked by exhaustion of intracellular calcium stores and inhibition of phospholipase C. It is concluded that linoleic acid stimulates [Ca(2+)](i) increase in islet β-cells through both extracellular calcium influx via TRP channels and calcium release from intracellular calcium stores.
