Role of G proteins in K(ATP) channel modulation by the neuropeptide somatostatin

B. Ribalet, S. Ciani, T. G. Hales, G. T. Eddlestone

Research output: Contribution to journalArticlepeer-review

3 Citations (Scopus)


Glucose-induced insulin secretion from the pancreatic β cell is initiated by a reduction of ATP-sensitive K+ [K(ATP)] channel activity. It was hypothesized that somatostatin (SRIF)-induced inhibition of insulin release is mediated via an increase in K(ATP) channel activity. Patch-clamp studies demonstrated that SRIF stimulates K(ATP) activity and further indicated that this mechanism involves a pertussis toxin-sensitive G protein. However, low concentrations of glucose reversed SRIF-mediated K(ATP) stimulation, indicating that inhibition of insulin secretion by SRIF is not mediated via its effect on K(ATP). On the basis of preliminary experiments it is proposed that the inhibition of secretion by SRIF is due to a G protein-induced decrease in calcium channel activity.

Original languageEnglish
Pages (from-to)37-40
Number of pages4
JournalBiomedical Research
Issue numberSUPPL. 2
Publication statusPublished - 1 Dec 1991

ASJC Scopus subject areas

  • Biochemistry, Genetics and Molecular Biology(all)


Dive into the research topics of 'Role of G proteins in K(ATP) channel modulation by the neuropeptide somatostatin'. Together they form a unique fingerprint.

Cite this