Journal
JOURNAL OF MOLECULAR ENDOCRINOLOGY
Volume 57, Issue 3, Pages F35-F39Publisher
BIOSCIENTIFICA LTD
DOI: 10.1530/JME-16-0106
Keywords
store-operated Ca2+ entry; TRPC1; STIM1; Orai1; insulin secretion; pancreatic beta-cells
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Funding
- Swiss National Science Foundation [31003A-155897]
- Agence Nationale de la Recherche [ANR-15-CE14-0005]
- Swiss National Science Foundation (SNF) [31003A_155897] Funding Source: Swiss National Science Foundation (SNF)
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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 beta-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 (K-ATP), 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.
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