Sabourin J Allagnat F 2016 Normal plasma glucose level is ensured by the action of insulin, the major hypoglycemic hormone. Therefore, it is not surprising that insulin release from pancreatic β-cells of the islets of Langerhans is controlled by an array of balanced mechanisms in which glucose plays the leading role. Glucose triggers insulin secretion through the well-described pathway of ATP-driven closure of ATP-sensitive potassium channels (KATP), depolarization of the plasma membrane, and opening of the voltage-dependent Ca2+ channels (VDCC). The subsequent rapid rise in cytoplasmic free Ca2+ concentration triggers insulin exocytosis. However, despite more than 40 years of investigation, certain aspects of the intracellular Ca2+ responses to glucose and secretagogues remain unexplained, suggesting the involvement of additional Ca2+ channels. Here, we discuss the emerging role of store-operated Ca2+ channels carried by Orai1 and transient receptor potential canonical 1 (TRPC1) proteins and regulated by the stromal interaction molecule 1 (STIM1) in the control of glucose-induced insulin secretion. The role of other voltage-independent cation channels formed by other members of the TRP channels family is also addressed. application/pdf https://sonar.ch/global/documents/259452 eng info:eu-repo/semantics/altIdentifier/doi/10.1530/JME-16-0106 info:eu-repo/semantics/altIdentifier/pmid/27589991 info:eu-repo/semantics/openAccess Journal of molecular endocrinology. - 2016 Orai1 STIM1 TRPC1 insulin secretion pancreatic β-cells store-operated Ca2+ entry Store-operated Ca2+ entry: a key component of the insulin secretion machinery. http://purl.org/coar/resource_type/c_6501