{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,11,26]],"date-time":"2025-11-26T04:50:49Z","timestamp":1764132649843},"reference-count":40,"publisher":"American Physiological Society","issue":"5","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Cell Physiology"],"published-print":{"date-parts":[[2012,3,1]]},"abstract":"<jats:p> While glucose-stimulated insulin secretion depends on Ca<jats:sup>2+<\/jats:sup> influx through voltage-gated Ca<jats:sup>2+<\/jats:sup> channels in the cell membrane of the pancreatic \u03b2-cell, there is also ample evidence for an important role of intracellular Ca<jats:sup>2+<\/jats:sup> stores in insulin secretion, particularly in relation to drug stimuli. We report here that thiopental, a common anesthetic agent, triggers insulin secretion from the intact pancreas and primary cultured rat pancreatic \u03b2-cells. We investigated the underlying mechanisms by measurements of whole cell K<jats:sup>+<\/jats:sup> and Ca<jats:sup>2+<\/jats:sup> currents, membrane potential, cytoplasmic Ca<jats:sup>2+<\/jats:sup> concentration ([Ca<jats:sup>2+<\/jats:sup>]<jats:sub>i<\/jats:sub>), and membrane capacitance. Thiopental-induced insulin secretion was first detected by enzyme-linked immunoassay, then further assessed by membrane capacitance measurement, which revealed kinetics distinct from glucose-induced insulin secretion. The thiopental-induced secretion was independent of cell membrane depolarization and closure of ATP-sensitive potassium (K<jats:sub>ATP<\/jats:sub>) channels. However, accompanied by the insulin secretion stimulated by thiopental, we recorded a significant intracellular [Ca<jats:sup>2+<\/jats:sup>] increase that was not from Ca<jats:sup>2+<\/jats:sup> influx across the cell membrane, but from intracellular Ca<jats:sup>2+<\/jats:sup> stores. The thiopental-induced [Ca<jats:sup>2+<\/jats:sup>]<jats:sub>i<\/jats:sub> rise in \u03b2-cells was sensitive to thapsigargin, a blocker of the endoplasmic reticulum Ca<jats:sup>2+<\/jats:sup> pump, as well as to heparin (0.1 mg\/ml) and 2-aminoethoxydiphenyl borate (2-APB; 100 \u03bcM), drugs that inhibit inositol 1,4,5-trisphosphate (IP<jats:sub>3<\/jats:sub>) binding to the IP<jats:sub>3<\/jats:sub> receptor, and to U-73122, a phospholipase C inhibitor, but insensitive to ryanodine. Thapsigargin also diminished thiopental-induced insulin secretion. Thus, we conclude that thiopental-induced insulin secretion is mediated by activation of the intracellular IP<jats:sub>3<\/jats:sub>-sensitive Ca<jats:sup>2+<\/jats:sup> store. <\/jats:p>","DOI":"10.1152\/ajpcell.00081.2011","type":"journal-article","created":{"date-parts":[[2011,12,2]],"date-time":"2011-12-02T12:39:23Z","timestamp":1322829563000},"page":"C796-C803","source":"Crossref","is-referenced-by-count":12,"title":["Thiopental-induced insulin secretion via activation of IP<sub>3<\/sub>-sensitive calcium stores in rat pancreatic \u03b2-cells"],"prefix":"10.1152","volume":"302","author":[{"given":"Hai-Qiang","family":"Dou","sequence":"first","affiliation":[{"name":"State Key Laboratory of Membrane Bioengineering and Peking-Tsinghua Center for Life Sciences, Institute of Molecular Medicine, Peking University, Beijing, China;"},{"name":"College of Engineering, Peking University, Beijing, China; 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