Glucose induces closure of single potassium channels in isolated rat pancreatic beta-cells
- PMID: 6095103
- DOI: 10.1038/312446a0
Glucose induces closure of single potassium channels in isolated rat pancreatic beta-cells
Abstract
The major physiological stimulus for the secretion of insulin from the pancreatic beta-cell is an increase in the plasma glucose concentration. It is well established that glucose-stimulated insulin secretion is associated with the appearance of electrical activity in the beta-cell; glucose concentrations above the threshold level for insulin release produce a slow membrane depolarization followed by either oscillatory bursts of action potentials (5-15 mM glucose) or continuous spiking (greater than 16 mM glucose). Tracer flux studies and microelectrode measurements using intact islets of Langerhans have indicated that the initial depolarization induced by glucose is caused by a decrease in the resting membrane permeability to potassium. Evidence also suggests that the electrical, ionic and secretory responses to glucose are mediated by the metabolism of the sugar within the beta-cell. By using cell-attached membrane patches from isolated rat pancreatic beta-cells, we have now identified a potassium channel (G-channel) that is active at the resting potential and is inhibited by glucose. Closure of this channel requires glucose metabolism. This is the first report of a potassium channel whose activity is modulated by glucose, and which may couple metabolic and ionic events involved in the secretion of insulin.
Similar articles
-
Properties of single potassium channels modulated by glucose in rat pancreatic beta-cells.J Physiol. 1988 Jun;400:501-27. doi: 10.1113/jphysiol.1988.sp017134. J Physiol. 1988. PMID: 2458459 Free PMC article.
-
A potassium channel modulated by glucose metabolism in rat pancreatic beta-cells.Adv Exp Med Biol. 1986;211:53-62. doi: 10.1007/978-1-4684-5314-0_4. Adv Exp Med Biol. 1986. PMID: 2440249 No abstract available.
-
Glucose and alpha-ketoisocaproate induce transient inward currents in rat pancreatic beta cells.Diabetologia. 1997 Jan;40(1):1-6. doi: 10.1007/s001250050635. Diabetologia. 1997. PMID: 9028711
-
Electrophysiology of islet cells.Adv Exp Med Biol. 2010;654:115-63. doi: 10.1007/978-90-481-3271-3_7. Adv Exp Med Biol. 2010. PMID: 20217497 Review.
-
Regulation of insulin release by ionic and electrical events in B cells.Horm Res. 1987;27(3):168-78. doi: 10.1159/000180806. Horm Res. 1987. PMID: 2447002 Review.
Cited by
-
Adenosine Triphosphate-Sensitive Potassium Currents in Heart Disease and Cardioprotection.Card Electrophysiol Clin. 2016 Jun;8(2):323-35. doi: 10.1016/j.ccep.2016.01.005. Epub 2016 Mar 19. Card Electrophysiol Clin. 2016. PMID: 27261824 Free PMC article. Review.
-
Mitochondrial Dysfunction, Oxidative Stress, and Inter-Organ Miscommunications in T2D Progression.Int J Mol Sci. 2024 Jan 25;25(3):1504. doi: 10.3390/ijms25031504. Int J Mol Sci. 2024. PMID: 38338783 Free PMC article. Review.
-
Effects of pinacidil, RP 49356 and nicorandil on ATP-sensitive potassium channels in insulin-secreting cells.Br J Pharmacol. 1990 Mar;99(3):487-92. doi: 10.1111/j.1476-5381.1990.tb12955.x. Br J Pharmacol. 1990. PMID: 2158844 Free PMC article.
-
Expression of transient receptor potential ankyrin 1 (TRPA1) and its role in insulin release from rat pancreatic beta cells.PLoS One. 2012;7(5):e38005. doi: 10.1371/journal.pone.0038005. Epub 2012 May 31. PLoS One. 2012. PMID: 22701540 Free PMC article.
-
Liquid junction potentials and small cell effects in patch-clamp analysis.J Membr Biol. 1991 Apr;121(2):101-17. doi: 10.1007/BF01870526. J Membr Biol. 1991. PMID: 1715403 Review. No abstract available.
Publication types
MeSH terms
Substances
LinkOut - more resources
Full Text Sources
Other Literature Sources
Medical
