A gene-family analysis of 61 genetic variants in the nicotinic acetylcholine receptor genes for insulin resistance and type 2 diabetes in American Indians.

MedStar author(s):
Citation: Diabetes. 61(7):1888-94, 2012 Jul.PMID: 22586585Institution: MedStar Health Research InstituteForm of publication: Journal ArticleMedline article type(s): Journal Article | Research Support, N.I.H., ExtramuralSubject headings: *Diabetes Mellitus, Type 2/ge [Genetics] | *Genetic Variation | *Indians, North American/ge [Genetics] | *Insulin Resistance/ge [Genetics] | *Receptors, Nicotinic/ge [Genetics] | Adult | Aged | Blood Glucose/an [Analysis] | Diabetes Mellitus, Type 2/ep [Epidemiology] | Female | Genetic Association Studies/sn [Statistics & Numerical Data] | Genetic Predisposition to Disease | Humans | Insulin/bl [Blood] | Male | Middle Aged | Pedigree | Polymorphism, Single Nucleotide | Smoking/ep [Epidemiology] | Smoking/ge [Genetics] | Young AdultLocal holdings: Available online from MWHC library: 1995 - present (after 3 months), Available in print through MWHC library: 1999 - 2006ISSN:
  • 0012-1797
Name of journal: DiabetesAbstract: Cigarette smoking is a risk factor for type 2 diabetes. Genetic variants in the nicotinic acetylcholine receptor (nAChR) genes have been associated with smoking phenotypes and are likely to influence diabetes. Although each single variant may have only a minor effect, the joint contribution of multiple single nucleotide polymorphisms (SNPs) to the occurrence of disease may be larger. In this study, we conducted a gene-family analysis to investigate the joint impact of 61 tag SNPs in 7 nAChRs genes on insulin resistance and type 2 diabetes in 3,665 American Indians recruited by the Strong Heart Family Study. Results show that although multiple SNPs showed marginal individual association with insulin resistance and type 2 diabetes, only a few can pass adjustment for multiple testing. However, a gene-family analysis considering the joint impact of all 61 SNPs reveals significant association of the nAChR gene family with both insulin resistance and type 2 diabetes (both P < 0.0001), suggesting that genetic variants in the nAChR genes jointly contribute to insulin resistance and type 2 diabetes among American Indians. The effects of these genetic variants on insulin resistance and diabetes are independent of cigarette smoking per se.All authors: Beebe LA, Best LG, Cole SA, Devereux RB, Haack K, Henderson JA, Henderson P, Howard BV, Lee ET, Yang J, Zhang Y, Zhao J, Zhu YDigital Object Identifier: Date added to catalog: 2013-09-17
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Item type Current library Collection Call number Status Date due Barcode
Journal Article MedStar Authors Catalog Article Available 22586585

Available online from MWHC library: 1995 - present (after 3 months), Available in print through MWHC library: 1999 - 2006

Cigarette smoking is a risk factor for type 2 diabetes. Genetic variants in the nicotinic acetylcholine receptor (nAChR) genes have been associated with smoking phenotypes and are likely to influence diabetes. Although each single variant may have only a minor effect, the joint contribution of multiple single nucleotide polymorphisms (SNPs) to the occurrence of disease may be larger. In this study, we conducted a gene-family analysis to investigate the joint impact of 61 tag SNPs in 7 nAChRs genes on insulin resistance and type 2 diabetes in 3,665 American Indians recruited by the Strong Heart Family Study. Results show that although multiple SNPs showed marginal individual association with insulin resistance and type 2 diabetes, only a few can pass adjustment for multiple testing. However, a gene-family analysis considering the joint impact of all 61 SNPs reveals significant association of the nAChR gene family with both insulin resistance and type 2 diabetes (both P < 0.0001), suggesting that genetic variants in the nAChR genes jointly contribute to insulin resistance and type 2 diabetes among American Indians. The effects of these genetic variants on insulin resistance and diabetes are independent of cigarette smoking per se.

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