| First Author | Puddu A | Year | 2008 |
| Journal | Biochem Biophys Res Commun | Volume | 375 |
| Issue | 2 | Pages | 235-7 |
| PubMed ID | 18703018 | Mgi Jnum | J:138985 |
| Mgi Id | MGI:3806935 | Doi | 10.1016/j.bbrc.2008.08.003 |
| Citation | Puddu A, et al. (2008) Caveolin-1 is essential for glimepiride-induced insulin secretion in the pancreatic betaTC-6 cell line. Biochem Biophys Res Commun 375(2):235-7 |
| abstractText | 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. |
