{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,2,20]],"date-time":"2026-02-20T08:57:24Z","timestamp":1771577844588,"version":"3.50.1"},"reference-count":22,"publisher":"American Diabetes Association","issue":"3","content-domain":{"domain":["diabetesjournals.org"],"crossmark-restriction":true},"short-container-title":[],"published-print":{"date-parts":[[2002,3,1]]},"abstract":"<jats:p>E23K, a common single nucleotide polymorphism in KIR6.2, the pore-forming subunit of pancreatic \u03b2-cell ATP-sensitive K+ channels, significantly enhanced open probability of these channels, thus reducing their sensitivity toward inhibitory ATP4\u2212 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 KIR6.2 in one allele and K in the other) and homozygous (K\/K; with K in position 23 of KIR6.2 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.<\/jats:p>","DOI":"10.2337\/diabetes.51.3.875","type":"journal-article","created":{"date-parts":[[2007,3,6]],"date-time":"2007-03-06T19:04:22Z","timestamp":1173207862000},"page":"875-879","update-policy":"https:\/\/doi.org\/10.2337\/ada-journal-policies","source":"Crossref","is-referenced-by-count":184,"title":["KIR6.2 Polymorphism Predisposes to Type 2 Diabetes by Inducing Overactivity of Pancreatic \u03b2-Cell ATP-Sensitive K+ Channels"],"prefix":"10.2337","volume":"51","author":[{"given":"Christina","family":"Schwanstecher","sequence":"first","affiliation":[{"name":"From the Institute of Pharmacology and Toxicology, University of Braunschweig, Braunschweig, Germany."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Ulrike","family":"Meyer","sequence":"additional","affiliation":[{"name":"From the Institute of Pharmacology and Toxicology, University of Braunschweig, Braunschweig, Germany."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Mathias","family":"Schwanstecher","sequence":"additional","affiliation":[{"name":"From the Institute of Pharmacology and Toxicology, University of Braunschweig, Braunschweig, Germany."}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"1167","reference":[{"key":"2022031223320254500_R1","doi-asserted-by":"crossref","unstructured":"Polonsky KS, Sturis J, Bell GI: Non-insulin-dependent diabetes mellitus\u2014a genetically programmed failure of the beta cell to compensate for insulin resistance. 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