skip to main content
Language:
Search Limited to: Search Limited to: Resource type Show Results with: Show Results with: Index

Block of K v 1.7 potassium currents increases glucose‐stimulated insulin secretion

Finol‐Urdaneta, Rocio K. ; Remedi, Maria S. ; Raasch, Walter ; Becker, Stefan ; Clark, Robert B. ; Strüver, Nina ; Pavlov, Evgeny ; Nichols, Colin G. ; French, Robert J. ; Terlau, Heinrich

EMBO Molecular Medicine, May 2012, Vol.4(5), pp.424-434 [Peer Reviewed Journal]

Full text available

Citations Cited by
  • Title:
    Block of K v 1.7 potassium currents increases glucose‐stimulated insulin secretion
  • Author: Finol‐Urdaneta, Rocio K. ; Remedi, Maria S. ; Raasch, Walter ; Becker, Stefan ; Clark, Robert B. ; Strüver, Nina ; Pavlov, Evgeny ; Nichols, Colin G. ; French, Robert J. ; Terlau, Heinrich
  • Description: Glucose‐stimulated insulin secretion (GSIS) relies on repetitive, electrical spiking activity of the beta cell membrane. Cyclic activation of voltage‐gated potassium channels (K) generates an outward, ‘delayed rectifier’ potassium current, which drives the repolarizing phase of each spike and modulates insulin release. Although several K channels are expressed in pancreatic islets, their individual contributions to GSIS remain incompletely understood. We take advantage of a naturally occurring cone‐snail peptide toxin, Conkunitzin‐S1 (Conk‐S1), which selectively blocks K1.7 channels to provide an intrinsically limited, finely graded control of total beta cell delayed rectifier current and hence of GSIS. Conk‐S1 increases GSIS in isolated rat islets, likely by reducing K1.7‐mediated delayed rectifier currents in beta cells, which yields increases in action potential firing and cytoplasmic free calcium. In rats, Conk‐S1 increases glucose‐dependent insulin secretion without decreasing basal glucose. Thus, we conclude that K1.7 contributes to the membrane‐repolarizing current of beta cells during GSIS and that block of this specific component of beta cell K current offers a potential strategy for enhancing GSIS with minimal risk of hypoglycaemia during metabolic disorders such as Type 2 diabetes.
  • Is Part Of: EMBO Molecular Medicine, May 2012, Vol.4(5), pp.424-434
  • Identifier: ISSN: 1757-4676 ; E-ISSN: 1757-4684 ; DOI: 10.1002/emmm.201200218
  • Subjects: Conkunitzin‐S1 ; Electrical Signalling ; Gsis ; Pancreas ; Potassium Channels
  • Language: English

Searching Remote Databases, Please Wait