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Nat. Rev. Endocrinol. doi:10.1038/nrendo.2016.86 Figure 3 Sulfonylureas, meglitinides and glucagon-like peptide 1 receptor agonists (GLP‑1RAs) act on pancreatic β cells to increase nutrient-induced insulin secretion Figure 3 | Sulfonylureas, meglitinides and glucagon-like peptide 1 receptor agonists (GLP-1RAs) act on pancreatic β cells to increase nutrient-induced insulin secretion. These agents bind to the cytosolic surface of the sulfonylurea receptor 1 (SUR1), which is part of the ATP-sensitive Kir6.2 potassium channel. Binding of the sulfonylurea or meglitinide closes the Kir6.2 channel, preventing potassium efflux and thereby depolarizing the plasma membrane. Depolarization opens local voltage-dependent calcium channels, increasing the influx of calcium and activating calcium-dependent signalling proteins that control insulin exocytosis. GLP-1RAs enhance nutrient-induced insulin release mainly via a cAMP–EPAC2-mediated potentiation of granule exocytosis. DAG, diacylglycerol; EPAC2, rap guanine nucleotide exchange factor 4; GLUT, glucose transporter isoform; IP3, inositol-1,4,5-trisphosphate; Rap1, Ras-related protein 1; PKA, protein kinase A; PKC, protein kinase C; PLC, phospholipase C. Tahrani, A. A. et al. (2016) Pharmacology and therapeutic implications of current drugs for type 2 diabetes mellitus Nat. Rev. Endocrinol. doi:10.1038/nrendo.2016.86