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KIR6.2 Polymorphism Predisposes to Type 2 Diabetes by Inducing Overactivity of Pancreatic β-Cell ATP-Sensitive K+ Channels

Diabetes (New York, N.Y.), 2002-03, Vol.51 (3), p.875-879 [Peer Reviewed Journal]

2002 INIST-CNRS ;ISSN: 0012-1797 ;EISSN: 1939-327X ;DOI: 10.2337/diabetes.51.3.875 ;PMID: 11872696 ;CODEN: DIAEAZ

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  • Title:
    KIR6.2 Polymorphism Predisposes to Type 2 Diabetes by Inducing Overactivity of Pancreatic β-Cell ATP-Sensitive K+ Channels
  • Author: SCHWANSTECHER, Christina ; MEYER, Ulrike ; SCHWANSTECHER, Mathias
  • Subjects: Biological and medical sciences
  • Is Part Of: Diabetes (New York, N.Y.), 2002-03, Vol.51 (3), p.875-879
  • Description: K IR 6.2 Polymorphism Predisposes to Type 2 Diabetes by Inducing Overactivity of Pancreatic β-Cell ATP-Sensitive K + Channels Christina Schwanstecher , Ulrike Meyer and Mathias Schwanstecher From the Institute of Pharmacology and Toxicology, University of Braunschweig, Braunschweig, Germany. Abstract E23K, a common single nucleotide polymorphism in K IR 6.2, the pore-forming subunit of pancreatic β-cell ATP-sensitive K + channels, significantly enhanced open probability of these channels, thus reducing their sensitivity toward inhibitory ATP 4− and increasing the threshold concentration for insulin release. Previous association studies and high allelic frequency suggest this effect to critically inhibit secretion and play a major role in pathogenesis of common type 2 diabetes. Based on evidence for functional relevance of E23K in both the heterozygous (E/K; with E in position 23 of K IR 6.2 in one allele and K in the other) and homozygous (K/K; with K in position 23 of K IR 6.2 in both alleles) genotype, we propose a model in which enhanced susceptibility to type 2 diabetes is associated with evolutionary advantage of the E/K state. Footnotes Address correspondence and reprint requests to Dr. M. Schwanstecher, Institut für Pharmakologie und Toxikologie, Universität Braunschweig, Mendelssohnstraβe 1, 38106 Braunschweig, Germany. E-mail: m.schwanstecher{at}tu-bs.de . Received for publication 18 December 2000 and accepted in revised form 29 November 2001. DMEM-HG, Dulbecco’s modified Eagle’s medium–high glucose; IC R2 , ATP concentration that suppresses spontaneous open probability to the threshold for insulin secretion (0.02); Δ I max , maximal increment of the spontaneous patch current; K ATP , ATP-sensitive K + channel; K IR 6.2 E23K , mutant isoform of K IR 6.2, with K instead of E in position 23; K IR 6.2 wt , wild-type isoform of K IR 6.2; P O, spontaneous open probability; SNP, single nucleotide polymorphism; SUR1, regulatory sulfonylurea receptor subunit-1. DIABETES
  • Publisher: Alexandria, VA: American Diabetes Association
  • Language: English
  • Identifier: ISSN: 0012-1797
    EISSN: 1939-327X
    DOI: 10.2337/diabetes.51.3.875
    PMID: 11872696
    CODEN: DIAEAZ
  • Source: Alma/SFX Local Collection
    ProQuest Central
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