Related Experiment Video
Updated: Oct 2, 2026

High-resolution Respirometry to Measure Mitochondrial Function of Intact Beta Cells in the Presence of Natural Compounds
Published on: January 23, 2018
K(IR)6.2 polymorphism predisposes to type 2 diabetes by inducing overactivity of pancreatic beta-cell ATP-sensitive
Christina Schwanstecher1, Ulrike Meyer, Mathias Schwanstecher
1Institute 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 beta-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.
Related Concept Videos
Type II Diabetes I: Introduction
Type I Diabetes II: Pathophysiology
Type II Diabetes II: Pathophysiology
Type I Diabetes I: Introduction
Diabetes Mellitus: Overview and Type I Subtype
Type 1 diabetes is an autoimmune disease in which the immune system mistakenly attacks and destroys the insulin-producing beta cells in the pancreas. As a result, the body is unable to produce sufficient insulin, and individuals with...
Diabetes Mellitus: Type 2 and Gestational
