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Original Articles

Amino Acid Polymorphisms in the ATP-Regulatable Inward Rectifier Kir6.2 and Their Relationships to Glucose- and Tolbutamide-Induced Insulin Secretion, the Insulin Sensitivity Index, and NIDDM

  1. Lars Hansen,
  2. Søren M Echwald,
  3. Torben Hansen,
  4. Søren A Urhammer,
  5. Jesper O Clausen and
  6. Oluf Pedersen
  1. Steno Diabetes Center and the Hagedorn Research Institute, Glostrup University Hospital Copenhagen, Denmark
  2. Center of Preventive Medicine, Glostrup University Hospital Copenhagen, Denmark
  1. Address correspondence and reprint requests to Dr. Lars Hansen, Steno Diabetes Center, Niels Steensens Vej 2, DK-2820 Gentofte, Denmark.
Diabetes 1997 Mar; 46(3): 508-512. https://doi.org/10.2337/diab.46.3.508
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Abstract

Kir6.2 is an inwardly rectifying potassium channel that is expressed in pancreatic (β-cells and cardiac and skeletal muscle. Expressed together with the highaffinity sulphonylurea receptor, it reconstitutes a sulphonylurea- and also ATP-sensitive potassium channel resembling the native (β-cell channel. The objective of this study was to search for mutations in the Kir6.2 gene that might be associated with NIDDM or related to altered insulin secretion, insulin action, or glucose metabolism in healthy subjects. Using polymerase chain reaction–single-strand conformation polymorphism analysis (PCR-SSCP) on genomic DNA from 69 Danish NIDDM patients and 66 matched control subjects, we report the finding of three missense polymorphisms in otherwise conserved codons and three silent polymorphisms in the gene encoding Kir6.2: codon 23 (GAG/AAG), Glu→Lys; codon 190 (GCT/GCC), Ala→Ala; codon 267 (CTC/CTG), Leu→Leu; codon 270 (CTG/GTG), Leu→Val; codon 337 (ATC/GTC), Ile→Val; codon 381 (AAG/AAA), Lys→Lys. The codon 23 and codon 337 amino acid polymorphisms were always coupled. The allelic frequencies of the polymorphisms were similar in NIDDM patients and control subjects. The amino acid polymorphisms were not associated with altered insulin secretion after intravenous glucose or tolbutamide injections or with altered glucose effectiveness in a phenotype study of 346 young healthy subjects. However, carriers of the maximal load of amino acid variants, the compound homozygous codon 23/337 and heterozygous codon 270, had on average a 62% higher insulin sensitivity index (P = 0.006), compared with noncarriers. We conclude that a combination of common Kir6.2 amino acid variants may contribute to the genetic background behind the large variation of the insulin sensitivity index in the general population.

  • Received May 28, 1996.
  • Revision received October 17, 1996.
  • Accepted October 17, 1996.
  • Copyright © 1997 by the American Diabetes Association
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March 1997, 46(3)
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Amino Acid Polymorphisms in the ATP-Regulatable Inward Rectifier Kir6.2 and Their Relationships to Glucose- and Tolbutamide-Induced Insulin Secretion, the Insulin Sensitivity Index, and NIDDM
Lars Hansen, Søren M Echwald, Torben Hansen, Søren A Urhammer, Jesper O Clausen, Oluf Pedersen
Diabetes Mar 1997, 46 (3) 508-512; DOI: 10.2337/diab.46.3.508

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Amino Acid Polymorphisms in the ATP-Regulatable Inward Rectifier Kir6.2 and Their Relationships to Glucose- and Tolbutamide-Induced Insulin Secretion, the Insulin Sensitivity Index, and NIDDM
Lars Hansen, Søren M Echwald, Torben Hansen, Søren A Urhammer, Jesper O Clausen, Oluf Pedersen
Diabetes Mar 1997, 46 (3) 508-512; DOI: 10.2337/diab.46.3.508
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