Scopoletin stimulates the secretion of insulin via a KATP channel-dependent pathway in INS-1 pancreatic β cells

Abstract Objectives In this study, we investigated whether scopoletin stimulated the secretion of insulin in pancreatic β cells as well as the underlying mechanism involved in this process. Methods We incubated the INS-1 pancreatic β cells with various concentrations of glucose (1.1, 5.6 or 16.7 mM) in the presence or absence of scopoletin. We then analysed the secretion of insulin in the cells treated with insulin secretion inhibitors or secretagogues. The intracellular influx of calcium induced by scopoletin was also analysed using the Fluo-2 AM dye. Key findings We found that scopoletin (1–20 µM) markedly induced the secretion of insulin in a glucose concentration-dependent manner compared with the control. At depolarizing concentrations of potassium chloride (KCl), scopoletin markedly enhanced the insulin secretion compared with the cells which were treated only with KCl. Moreover, the treatment with diazoxide-opening K+ATP channel and verapamil blocking Ca2+ channel significantly decreased the scopoletin-induced increase in insulin secretion. After the pre-treatment of cells with a Ca2+ fluorescent dye, treatment with 20 µM scopoletin resulted in a significant increase in the influx of intracellular Ca2+, exhibiting fluorescence changes in various spectra. Conclusions Scopoletin stimulates the secretion of insulin via a K+ATP channel-dependent pathway in the INS-1 pancreatic β cells.