Cellular and Molecular Life Sciences

, Volume 71, Issue 21, pp 4149–4177

Ionic mechanisms in pancreatic β cell signaling

  • Shao-Nian Yang
  • Yue Shi
  • Guang Yang
  • Yuxin Li
  • Jia Yu
  • Per-Olof Berggren

DOI: 10.1007/s00018-014-1680-6

Cite this article as:
Yang, SN., Shi, Y., Yang, G. et al. Cell. Mol. Life Sci. (2014) 71: 4149. doi:10.1007/s00018-014-1680-6


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+, Ca2+ 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 Ca2+ (CaV) channel-mediated Ca2+ 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. Ca2+ 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 Ca2+ 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.


Calcium mobilization Electrophysiology Exocytosis Ion channel Pancreatic endocrine cell Protein kinase 



α1-interaction domain


Cytosolic free Ca2+ concentration


Calcium/calmodulin-dependent kinase II


Voltage-gated Ca2+


CaV1 channel conductance


KATP channel conductance


KV2.1 channel conductance


ATP-sensitive K+


Voltage-gated K+


Potassium inward rectifier


Nucleotide-binding fold


Phosphatidylinositol 4,5-bisphosphate


Protein kinase A


Protein kinase C


Membrane-associated pore loop


Sulfonylurea receptor


Transmembrane domain

Copyright information

© Springer Basel 2014

Authors and Affiliations

  • Shao-Nian Yang
    • 1
    • 3
  • Yue Shi
    • 1
  • Guang Yang
    • 1
    • 2
  • Yuxin Li
    • 3
  • Jia Yu
    • 1
  • Per-Olof Berggren
    • 1
  1. 1.The Rolf Luft Research Center for Diabetes and EndocrinologyKarolinska InstitutetStockholmSweden
  2. 2.Jilin Academy of Traditional Chinese MedicineChangchunChina
  3. 3.National Engineering Laboratory for Druggable Gene and Protein ScreeningNortheast Normal UniversityChangchunChina

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