Does galanin inhibit insulin secretion by opening of the ATP-regulated K+ channel in the β-cell?

Bo Ahrén, Per Olof Berggren, Krister Bokvist, Patrik Rorsman

Research output: Contribution to journalArticle

33 Citations (Scopus)

Abstract

The intrapancreatic neuropeptide galanin potently inhibits glucose-induced insulin secretion. This effect is in part due to a repolarization of the β-cells and ensuring reduction in the cytoplasmic free Ca2+ concentration, [Ca2+]i. We propose that galanin inhibition of β-cell action potentials is associated with the appearance of ATP-regulated K+ channels. Galanin opens K+ channels in a patch membrane when applied to the external solution in the cell-attached patch configuration. However, galanin does not detectably increase K+ permeability during whole-cell experiments, even when GTP was included in the internal solution. Our findings are not consistent with a direct effect of galanin on the K+ channels, but rather indicate that the effect of the neuropeptide is mediated by some intracellular coupling factor(s).

Original languageEnglish
Pages (from-to)453-457
Number of pages5
JournalPeptides
Volume10
Issue number2
DOIs
StatePublished - Jan 1 1989
Externally publishedYes

Fingerprint

Galanin
Adenosine Triphosphate
Insulin
Neuropeptides
Guanosine Triphosphate
Action Potentials
Permeability
Membranes
Glucose
Experiments

Keywords

  • Galanin
  • Insulin secretion
  • K channels
  • β-Cells

ASJC Scopus subject areas

  • Biochemistry
  • Endocrinology
  • Physiology
  • Cellular and Molecular Neuroscience

Cite this

Does galanin inhibit insulin secretion by opening of the ATP-regulated K+ channel in the β-cell? / Ahrén, Bo; Berggren, Per Olof; Bokvist, Krister; Rorsman, Patrik.

In: Peptides, Vol. 10, No. 2, 01.01.1989, p. 453-457.

Research output: Contribution to journalArticle

Ahrén, Bo ; Berggren, Per Olof ; Bokvist, Krister ; Rorsman, Patrik. / Does galanin inhibit insulin secretion by opening of the ATP-regulated K+ channel in the β-cell?. In: Peptides. 1989 ; Vol. 10, No. 2. pp. 453-457.
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