Linked Life Data

12196481

Source:http://linkedlifedata.com/resource/pubmed/id/12196481

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pubmed-article:12196481pubmed:abstractTextGenetic factors play an important role in the pathogenesis of type 2 diabetes. The relevance to type 2 diabetes of the common polymorphism Glu23Lys in the potassium inward rectifier 6.2 (KIR6.2) gene is still controversial. The aim of this study was to assess whether this polymorphism influences beta-cell function, alpha-cell function, or insulin action. We therefore studied 298 nondiabetic subjects using an oral glucose tolerance test (OGTT) and 75 nondiabetic subjects using a hyperglycemic clamp (10 mmol/l) with additional glucagon-like peptide (GLP)-1 and arginine stimulation. The prevalence of the Lys allele was approximately 37%, and the Lys allele was associated with higher incremental plasma glucose during the OGTT (P = 0.03, ANOVA). Neither first- nor second-phase glucose-stimulated C-peptide secretion was affected by the presence of the polymorphism; nor were maximal glucose-, GLP-1-, or arginine-induced C-peptide secretion rates; nor was insulin sensitivity (all P > 0.7). However, the relative decrease in plasma glucagon concentrations during the 10 min after the glucose challenge was reduced in carriers of the Lys allele (10 +/- 3% decrease from baseline in Lys/Lys, 18 +/- 2% in Glu/Lys, and 20 +/- 2% in Glu/Glu; P = 0.01, ANOVA). In conclusion, our findings suggest that the common Glu23Lys polymorphism in KIR6.2 is not necessarily associated with beta-cell dysfunction or insulin resistance but with diminished suppression of glucagon secretion in response to hyperglycemia. Our findings thus confirm its functional relevance for glucose metabolism in humans.lld:pubmed
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pubmed-article:12196481pubmed:dateRevised2011-11-17lld:pubmed
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pubmed-article:12196481pubmed:articleTitleThe prevalent Glu23Lys polymorphism in the potassium inward rectifier 6.2 (KIR6.2) gene is associated with impaired glucagon suppression in response to hyperglycemia.lld:pubmed
pubmed-article:12196481pubmed:affiliationDepartment of Endocrinology, Metabolism and Pathobiochemistry, Medizinische Klinik, Eberhard-Karls-Universität, Tübingen, Germany.lld:pubmed
pubmed-article:12196481pubmed:publicationTypeJournal Articlelld:pubmed
pubmed-article:12196481pubmed:publicationTypeResearch Support, Non-U.S. Gov'tlld:pubmed
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