title: Ionic mechanisms in pancreatic β cell signaling.
abstract: The function and survival of pancreatic β cells critically rely on complex electrical signaling systems composed of a series of ionic events, namely fluxes of K(+), Na(+), Ca(2+) and Cl(-) across the β cell membranes. These electrical signaling systems not only sense events occurring in the extracellular space and intracellular milieu of pancreatic islet cells, but also control different β cell activities, most notably glucose-stimulated insulin secretion. Three major ion fluxes including K(+) efflux through ATP-sensitive K(+) (KATP) channels, the voltage-gated Ca(2+) (CaV) channel-mediated Ca(2+) influx and K(+) efflux through voltage-gated K(+) (KV) channels operate in the β cell. These ion fluxes set the resting membrane potential and the shape, rate and pattern of firing of action potentials under different metabolic conditions. The KATP channel-mediated K(+) efflux determines the resting membrane potential and keeps the excitability of the β cell at low levels. Ca(2+) influx through CaV1 channels, a major type of β cell CaV channels, causes the upstroke or depolarization phase of the action potential and regulates a wide range of β cell functions including the most elementary β cell function, insulin secretion. K(+) efflux mediated by KV2.1 delayed rectifier K(+) channels, a predominant form of β cell KV channels, brings about the downstroke or repolarization phase of the action potential, which acts as a brake for insulin secretion owing to shutting down the CaV channel-mediated Ca(2+) entry. These three ion channel-mediated ion fluxes are the most important ionic events in β cell signaling. This review concisely discusses various ionic mechanisms in β cell signaling and highlights KATP channel-, CaV1 channel- and KV2.1 channel-mediated ion fluxes.
authors: The Rolf Luft Research Center for Diabetes and Endocrinology, Karolinska Institutet, SE-171 76, Stockholm, Sweden, shao-nian.yang@ki.se.
authors: Shao-Nian
authors: SN
authors: Yang
authors: Yue
authors: Y
authors: Shi
authors: Guang
authors: G
authors: Yang
authors: Yuxin
authors: Y
authors: Li
authors: Jia
authors: J
authors: Yu
authors: Per-Olof
authors: PO
authors: Berggren
mesh_terms: D000200:Action Potentials; D000255:Adenosine Triphosphate / Q000378:metabolism; D000818:Animals; D002118:Calcium / Q000378:metabolism; D015220:Calcium Channels / Q000378:metabolism*; D002462:Cell Membrane / Q000378:metabolism; D005089:Exocytosis; D006801:Humans; D007328:Insulin / Q000378:metabolism; D050417:Insulin-Secreting Cells / Q000166:cytology*; D007477:Ions / Q000378:metabolism; D008564:Membrane Potentials; D011188:Potassium / Q000378:metabolism; D015221:Potassium Channels / Q000378:metabolism*; D015398:Signal Transduction
chemical_list: D015220:Calcium Channels; D007328:Insulin; D007477:Ions; D015221:Potassium Channels; D000255:Adenosine Triphosphate; D011188:Potassium; D002118:Calcium