Statements in which the resource exists.
SubjectPredicateObjectContext
pubmed-article:12502511rdf:typepubmed:Citationlld:pubmed
pubmed-article:12502511lifeskim:mentionsumls-concept:C0005612lld:lifeskim
pubmed-article:12502511lifeskim:mentionsumls-concept:C0032659lld:lifeskim
pubmed-article:12502511lifeskim:mentionsumls-concept:C0011860lld:lifeskim
pubmed-article:12502511lifeskim:mentionsumls-concept:C1337112lld:lifeskim
pubmed-article:12502511lifeskim:mentionsumls-concept:C0242827lld:lifeskim
pubmed-article:12502511lifeskim:mentionsumls-concept:C1710347lld:lifeskim
pubmed-article:12502511lifeskim:mentionsumls-concept:C0023746lld:lifeskim
pubmed-article:12502511lifeskim:mentionsumls-concept:C0456387lld:lifeskim
pubmed-article:12502511lifeskim:mentionsumls-concept:C1882417lld:lifeskim
pubmed-article:12502511lifeskim:mentionsumls-concept:C0722638lld:lifeskim
pubmed-article:12502511pubmed:issue1lld:pubmed
pubmed-article:12502511pubmed:dateCreated2002-12-27lld:pubmed
pubmed-article:12502511pubmed:abstractTextThe insulin gene variable number tandem repeat (INS-VNTR) is proposed to exert pleiotropic genetic effects on birth weight and diabetes susceptibility. In our study, we examined the influence of a polymorphism in tight linkage disequilibrium with INS-VNTR (-23Hph1) on birth weight and type 2 diabetes in the Pima population. A parent-offspring "trio" design was used to assess parent-of-origin effects and population stratification. The presence of the -23Hph1 T-allele was associated with lower birth weight (n = 192; -140 g per copy of the T-allele; P = 0.04), even after adjustment for effects of population stratification (P = 0.03). The effects of paternally transmitted T-alleles were greater than those of maternally transmitted alleles (paternally transmitted: -250 g, P = 0.05; maternally transmitted: -111 g, P = 0.43), but this difference was not statistically significant (P = 0.50). The -23Hph1 T-allele was associated with an increased prevalence of type 2 diabetes (P = 0.009), which family-based association analysis suggested was attributable to population structure (P = 0.04) without significant evidence of linkage disequilibrium between diabetes prevalence and genotype (P = 0.86). Thus allelic variation of the INS gene is associated with lower birth weight and increased prevalence of type 2 diabetes. Significant linkage disequilibrium was found between -23Hph1 and birth weight but not type 2 diabetes, an observation that supports a potential functional role of INS polymorphisms in the regulation of birth weight.lld:pubmed
pubmed-article:12502511pubmed:languageenglld:pubmed
pubmed-article:12502511pubmed:journalhttp://linkedlifedata.com/r...lld:pubmed
pubmed-article:12502511pubmed:citationSubsetAIMlld:pubmed
pubmed-article:12502511pubmed:chemicalhttp://linkedlifedata.com/r...lld:pubmed
pubmed-article:12502511pubmed:statusMEDLINElld:pubmed
pubmed-article:12502511pubmed:monthJanlld:pubmed
pubmed-article:12502511pubmed:issn0012-1797lld:pubmed
pubmed-article:12502511pubmed:authorpubmed-author:LindsayRobert...lld:pubmed
pubmed-article:12502511pubmed:authorpubmed-author:HansonRobert...lld:pubmed
pubmed-article:12502511pubmed:authorpubmed-author:KnowlerWillia...lld:pubmed
pubmed-article:12502511pubmed:authorpubmed-author:BaierLeslie...lld:pubmed
pubmed-article:12502511pubmed:authorpubmed-author:BennettPeter...lld:pubmed
pubmed-article:12502511pubmed:authorpubmed-author:WiedrichChris...lld:pubmed
pubmed-article:12502511pubmed:issnTypePrintlld:pubmed
pubmed-article:12502511pubmed:volume52lld:pubmed
pubmed-article:12502511pubmed:ownerNLMlld:pubmed
pubmed-article:12502511pubmed:authorsCompleteYlld:pubmed
pubmed-article:12502511pubmed:pagination187-93lld:pubmed
pubmed-article:12502511pubmed:dateRevised2011-11-17lld:pubmed
pubmed-article:12502511pubmed:meshHeadingpubmed-meshheading:12502511...lld:pubmed
pubmed-article:12502511pubmed:meshHeadingpubmed-meshheading:12502511...lld:pubmed
pubmed-article:12502511pubmed:meshHeadingpubmed-meshheading:12502511...lld:pubmed
pubmed-article:12502511pubmed:meshHeadingpubmed-meshheading:12502511...lld:pubmed
pubmed-article:12502511pubmed:meshHeadingpubmed-meshheading:12502511...lld:pubmed
pubmed-article:12502511pubmed:meshHeadingpubmed-meshheading:12502511...lld:pubmed
pubmed-article:12502511pubmed:meshHeadingpubmed-meshheading:12502511...lld:pubmed
pubmed-article:12502511pubmed:meshHeadingpubmed-meshheading:12502511...lld:pubmed
pubmed-article:12502511pubmed:meshHeadingpubmed-meshheading:12502511...lld:pubmed
pubmed-article:12502511pubmed:meshHeadingpubmed-meshheading:12502511...lld:pubmed
pubmed-article:12502511pubmed:meshHeadingpubmed-meshheading:12502511...lld:pubmed
pubmed-article:12502511pubmed:meshHeadingpubmed-meshheading:12502511...lld:pubmed
pubmed-article:12502511pubmed:meshHeadingpubmed-meshheading:12502511...lld:pubmed
pubmed-article:12502511pubmed:year2003lld:pubmed
pubmed-article:12502511pubmed:articleTitleThe insulin gene variable number tandem repeat class I/III polymorphism is in linkage disequilibrium with birth weight but not Type 2 diabetes in the Pima population.lld:pubmed
pubmed-article:12502511pubmed:affiliationNational Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Phoenix, Arizona 85014, USA.lld:pubmed
pubmed-article:12502511pubmed:publicationTypeJournal Articlelld:pubmed
http://linkedlifedata.com/r...pubmed:referesTopubmed-article:12502511lld:pubmed
http://linkedlifedata.com/r...pubmed:referesTopubmed-article:12502511lld:pubmed
http://linkedlifedata.com/r...pubmed:referesTopubmed-article:12502511lld:pubmed
http://linkedlifedata.com/r...pubmed:referesTopubmed-article:12502511lld:pubmed