Glucose sensing of individual pancreatic β-cells involves transitions between steady-state and oscillatory cytoplasmic Ca2+
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Amplification of insulin secretion by acetylcholine or phorbol ester is independent of β-cell microfilaments and distinct from metabolic amplification
2013, Molecular and Cellular EndocrinologyCitation Excerpt :The transient post-stimulation decrease is due to membrane repolarization by activation of the electrogenic Na+ pump. In contrast, PMA caused a stable decrease of [Ca2+]c to a lower level than the peak of glucose-induced [Ca2+]c oscillations, as already observed in mouse single β-cells (Grapengiesser et al., 1992; Kindmark et al., 1992) and intact islets (Gao et al., 1994). We further show that PMA also decreased [Ca2+]c during first phase of the response to glucose and both phases of the response to tolbutamide.
Pulses of external ATP aid to the synchronization of pancreatic β-cells by generating premature Ca<sup>2+</sup> oscillations
2004, Biochemical PharmacologyCitation Excerpt :The inhibitory component in the ATP action may reflect an enhanced extrusion of Ca2+, mediated by activation of protein kinase C, and/or closure of the voltage-dependent Ca2+ channels. Evidence has been provided that stimulation of protein kinase C sometimes results in a disappearance of the oscillations with a steady-state of [Ca2+]i slightly above the basal level [39]. Moreover, it has been reported that external ATP acts as a G-protein-coupled inhibitor of L-type Ca2+ channels in rat β-cells [40] but not in mouse β-cells [22].
Effects of ELF and static magnetic fields on calcium oscillations in islets of Langerhans
2003, BioelectrochemistrySignal Transduction. Regulation of Insulin Secretion by Changes in CA<sup>2+</sup> Concentration and Action in Pancreatic β-Cells
1999, Advances in Molecular and Cell BiologyCrosstalk between the cAMP and inositol trisphosphate-signalling pathways in pancreatic β-cells
1996, Archives of Biochemistry and Biophysics