Source:http://linkedlifedata.com/resource/pubmed/id/16855181
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| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:issue |
5
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| pubmed:dateCreated |
2006-7-20
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| pubmed:abstractText |
Elevated plasma levels of plasminogen activator inhibitor-1 (PAI-1) increase risk for type 2 diabetes. The PAI-1 4G/5G polymorphism is a major genetic determinant of plasma PAI-1 levels, with 4G/4G homozygotes having elevated PAI-1 levels relative to 5G allele carriers. These observations suggest the hypothesis that the PAI-1 4G/5G polymorphism could be a genetic risk factor for diabetes. We tested this hypothesis among 2169 participants of the Framingham Offspring Study followed for seven examinations over 26 years for 216 cases of type 2 diabetes. PAI-1 4G/4G homozygotes (genotype frequency, 27.4%) were not at significantly (p > 0.05) increased risk of incident diabetes compared with 5G allele carriers and did not have elevated levels of diabetes-related quantitative traits including BMI, fasting plasma glucose, or fasting insulin. In proportional hazards regression models accounting for correlation among siblings, with the 5G/5G genotype as the referent, the hazard ratio for incident diabetes for 4G/5G carriers was 0.93 (95% confidence interval, 0.68 to 1.28) and for 4G/4G carriers was 1.20 (95% confidence interval, 0.83 to 1.92). Results were not altered by further adjustment for sex or levels of BMI, triglycerides, or PAI-1. We conclude that the PAI-1 4G/5G polymorphism is not an important genetic risk factor for type 2 diabetes in this community-based sample. Elevated PAI-1 levels may be associated with an increased risk for diabetes as a marker for underlying endothelial dysfunction rather than by a direct effect of genetically mediated elevated levels.
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| pubmed:grant | |
| pubmed:language |
eng
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| pubmed:journal | |
| pubmed:citationSubset |
IM
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| pubmed:chemical | |
| pubmed:status |
MEDLINE
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| pubmed:month |
May
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| pubmed:issn |
1930-7381
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| pubmed:author |
pubmed-author:CupplesL AdrienneLA,
pubmed-author:DupuisJoséeJ,
pubmed-author:FengDaliD,
pubmed-author:FoxCaroline SCS,
pubmed-author:GabrielStacey BSB,
pubmed-author:HerbertAlan GAG,
pubmed-author:KathiresanSekarS,
pubmed-author:LarsonMartin GMG,
pubmed-author:LiuChunyuC,
pubmed-author:O'DonnellChristopher JCJ,
pubmed-author:SpangenbergEE,
pubmed-author:ToflerGeoffrey HGH,
pubmed-author:WilsonPeter W FPW,
pubmed-author:YangQiongQ
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| pubmed:issnType |
Print
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| pubmed:volume |
14
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| pubmed:owner |
NLM
|
| pubmed:authorsComplete |
Y
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| pubmed:pagination |
753-8
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| pubmed:dateRevised |
2011-11-17
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| pubmed:meshHeading |
pubmed-meshheading:16855181-Adult,
pubmed-meshheading:16855181-Aged,
pubmed-meshheading:16855181-Aged, 80 and over,
pubmed-meshheading:16855181-Blood Glucose,
pubmed-meshheading:16855181-Body Mass Index,
pubmed-meshheading:16855181-Cohort Studies,
pubmed-meshheading:16855181-Diabetes Mellitus, Type 2,
pubmed-meshheading:16855181-Female,
pubmed-meshheading:16855181-Gene Frequency,
pubmed-meshheading:16855181-Genotype,
pubmed-meshheading:16855181-Humans,
pubmed-meshheading:16855181-Insulin,
pubmed-meshheading:16855181-Male,
pubmed-meshheading:16855181-Middle Aged,
pubmed-meshheading:16855181-Phenotype,
pubmed-meshheading:16855181-Plasminogen Activator Inhibitor 1,
pubmed-meshheading:16855181-Polymorphism, Genetic,
pubmed-meshheading:16855181-Proportional Hazards Models,
pubmed-meshheading:16855181-Risk Factors
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| pubmed:year |
2006
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| pubmed:articleTitle |
PAI-1 Gene 4G/5G polymorphism and risk of type 2 diabetes in a population-based sample.
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| pubmed:affiliation |
General Medicine Division, Department of Medicine, Massachusetts General Hospital and Harvard Medical School, Boston, MA 02114, USA. jmeigs@partners.org
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| pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't,
Research Support, N.I.H., Extramural
|