Source:http://linkedlifedata.com/resource/pubmed/id/16443791
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
2
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pubmed:dateCreated |
2006-1-30
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pubmed:abstractText |
Endothelial dysfunction may precede development of type 2 diabetes. We tested the hypothesis that elevated levels of hemostatic markers of endothelial dysfunction, plasminogen activator inhibitor-1 (PAI-1) antigen, and von Willebrand factor (vWF) antigen predicted incident diabetes independent of other diabetes risk factors. We followed 2,924 Framingham Offspring subjects (54% women, mean age 54 years) without diabetes at baseline (defined by treatment, fasting plasma glucose > or =7 or 2-h postchallenge glucose > or =11.1 mmol/l) over 7 years for new cases of diabetes (treatment or fasting plasma glucose > or =7.0 mmol/l). We used a series of regression models to estimate relative risks for diabetes per interquartile range (IQR) increase in PAI-1 (IQR 16.8 ng/ml) and vWF (IQR 66.8% of control) conditioned on baseline characteristics. Over follow-up, there were 153 new cases of diabetes. Age- and sex-adjusted relative risks of diabetes were 1.55 per IQR for PAI-1 (95% CI 1.41-1.70) and 1.49 for vWF (1.21-1.85). These effects remained after further adjustment for diabetes risk factors (including physical activity; HDL cholesterol, triglyceride, and blood pressure levels; smoking; parental history of diabetes; use of alcohol, nonsteroidal anti-inflammatory drugs, exogenous estrogen, or hypertension therapy; and impaired glucose tolerance), waist circumference, homeostasis model assessment of insulin resistance, and inflammation (assessed by levels of C-reactive protein): the adjusted relative risks were 1.18 per IQR for PAI-1 (1.01-1.37) and 1.39 for vWF (1.09-1.77). We conclude that in this community-based sample, plasma markers of endothelial dysfunction increased risk of incident diabetes independent of other diabetes risk factors including obesity, insulin resistance, and inflammation.
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pubmed:grant | |
pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
AIM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Biological Markers,
http://linkedlifedata.com/resource/pubmed/chemical/C-Reactive Protein,
http://linkedlifedata.com/resource/pubmed/chemical/Plasminogen Activator Inhibitor 1,
http://linkedlifedata.com/resource/pubmed/chemical/SERPINE1 protein, human,
http://linkedlifedata.com/resource/pubmed/chemical/von Willebrand Factor
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pubmed:status |
MEDLINE
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pubmed:month |
Feb
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pubmed:issn |
0012-1797
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pubmed:author |
pubmed-author:BenjaminEmelia JEJ,
pubmed-author:D'AgostinoRalph BRB,
pubmed-author:FoxCaroline SCS,
pubmed-author:LipinskaIzabelaI,
pubmed-author:NathanDavid MDM,
pubmed-author:O'donnellChristopher JCJ,
pubmed-author:SpangenbergEE,
pubmed-author:SullivanLisa MLM,
pubmed-author:ToflerGeoffrey HGH,
pubmed-author:WilsonPeter W FPW
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pubmed:issnType |
Print
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pubmed:volume |
55
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
530-7
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pubmed:dateRevised |
2007-11-14
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pubmed:meshHeading |
pubmed-meshheading:16443791-Adult,
pubmed-meshheading:16443791-Biological Markers,
pubmed-meshheading:16443791-C-Reactive Protein,
pubmed-meshheading:16443791-Diabetes Mellitus, Type 2,
pubmed-meshheading:16443791-Endothelium, Vascular,
pubmed-meshheading:16443791-Female,
pubmed-meshheading:16443791-Hemostasis,
pubmed-meshheading:16443791-Humans,
pubmed-meshheading:16443791-Inflammation,
pubmed-meshheading:16443791-Insulin Resistance,
pubmed-meshheading:16443791-Male,
pubmed-meshheading:16443791-Massachusetts,
pubmed-meshheading:16443791-Middle Aged,
pubmed-meshheading:16443791-Obesity,
pubmed-meshheading:16443791-Plasminogen Activator Inhibitor 1,
pubmed-meshheading:16443791-Risk Factors,
pubmed-meshheading:16443791-von Willebrand Factor
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pubmed:year |
2006
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pubmed:articleTitle |
Hemostatic markers of endothelial dysfunction and risk of incident type 2 diabetes: the Framingham Offspring Study.
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pubmed:affiliation |
General Medicine Division, Department of Medicine, Massachusetts General Hospital and Harvard Medical School, Boston, 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
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