PubMed 18703018
Referenced in: none
Automatically associated channels: Kir6.2
Title: Caveolin-1 is essential for glimepiride-induced insulin secretion in the pancreatic betaTC-6 cell line.
Authors: A Puddu, B Salani, R Cordera, G L Viviani, D Maggi
Journal, date & volume: Biochem. Biophys. Res. Commun., 2008 Oct 17 , 375, 235-7
PubMed link: http://www.ncbi.nlm.nih.gov/pubmed/18703018
Abstract
The K(ATP) channels play a pivotal role in the complex mechanism of insulin secretion. K(ATP) channels represent the target of sulphonylureas, a class of drugs widely used in type 2 diabetes to stimulate insulin secretion. We previously showed that caveolin-1 depletion impairs action of the sulphonylurea glimepiride in human endothelial cells. The aim of this work was to investigate the possible role of caveolin-1 in glimepiride-induced insulin secretion. Caveolin-1 was depleted using siRNA method in the pancreatic betaTC-6 cell line. Then stimulation of insulin secretion was performed with different secretagogues (glucose, KCl, and glimepiride). Here, we show that betaTC-6 caveolin-1 depleted cells maintained high rate of insulin secretion after KCl, but not after glucose and glimepiride stimulation. Moreover, we find a direct interaction between caveolin-1 and Kir6.2, one of the K(ATP) channel subunit. These results demonstrate that Cav-1 plays a critical role for glucose and sulfonylurea-stimulated insulin secretion.