Somatostatin induces hyperpolarization in pancreatic islet alpha cells by activating a G protein-gated K+ channel

FEBS Lett. 1999 Feb 12;444(2-3):265-9. doi: 10.1016/s0014-5793(99)00076-9.


Somatostatin inhibits glucagon-secretion from pancreatic alpha cells but its underlying mechanism is unknown. In mouse alpha cells, we found that somatostatin induced prominent hyperpolarization by activating a K+ channel, which was unaffected by tolbutamide but prevented by pre-treating the cells with pertussis toxin. The K+ channel was activated by intracellular GTP (with somatostatin), GTPgammaS or Gbetagamma subunits. It was thus identified as a G protein-gated K+ (K(G)) channel. RT-PCR and immunohistochemical analyses suggested the K(G) channel to be composed of Kir3.2c and Kir3.4. This study identified a novel ionic mechanism involved in somatostatin-inhibition of glucagon-secretion from pancreatic alpha cells.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Acetylcholine / pharmacology
  • Animals
  • Electrophysiology
  • Female
  • G Protein-Coupled Inwardly-Rectifying Potassium Channels
  • GTP-Binding Proteins / metabolism*
  • Glucagon / metabolism
  • Guanosine Triphosphate / pharmacology
  • Immunohistochemistry
  • Ion Channel Gating / physiology*
  • Islets of Langerhans / drug effects*
  • Mice
  • Mice, Inbred Strains
  • Patch-Clamp Techniques
  • Pertussis Toxin
  • Potassium Channels / genetics
  • Potassium Channels / metabolism*
  • Potassium Channels, Inwardly Rectifying*
  • RNA, Messenger / metabolism
  • Somatostatin / pharmacology*
  • Tolbutamide / pharmacology
  • Virulence Factors, Bordetella / pharmacology


  • G Protein-Coupled Inwardly-Rectifying Potassium Channels
  • Potassium Channels
  • Potassium Channels, Inwardly Rectifying
  • RNA, Messenger
  • Virulence Factors, Bordetella
  • Somatostatin
  • Guanosine Triphosphate
  • Glucagon
  • Tolbutamide
  • Pertussis Toxin
  • GTP-Binding Proteins
  • Acetylcholine