Diabetes
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
QUICK SEARCH:   [advanced]


     

This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Purchase Article
Right arrow View Shopping Cart
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow Request Permissions
Citing Articles
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Rose, C. S.
Right arrow Articles by Hansen, T.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Rose, C. S.
Right arrow Articles by Hansen, T.
Social Bookmarking
Add to CiteULike   Add to Del.icio.us   Add to Digg   Add to Reddit   Add to Technorati  
What's this?

Diabetes 54:3026-3031, 2005
© 2005 by the American Diabetes Association, Inc.

Brief Genetics Reports

A –30G>A Polymorphism of the ß-Cell–Specific Glucokinase Promoter Associates With Hyperglycemia in the General Population of Whites

Christian S. Rose1, Jakob Ek1, Søren A. Urhammer1, Charlotte Glümer1,2, Knut Borch-Johnsen1,3, Torben Jørgensen2, Oluf Pedersen1,3, and Torben Hansen1

1 Steno Diabetes Center and Hagedorn Research Institute, Copenhagen, Denmark
2 Centre of Preventive Medicine, Glostrup University Hospital, Glostrup, Denmark
3 Faculty of Health Science, University of Aarhus, Aarhus, Denmark

A graded relationship has been reported between fasting and postprandial plasma glucose levels and the subsequent risk of cardiovascular morbidity and mortality. We hypothesized that the GCK –30G>A promoter polymorphism is associated with elevated glycemia in the middle-aged general population of whites, as well as with features of the World Health Organization (WHO)-defined metabolic syndrome. The GCK –30G>A polymorphism was genotyped in the population-based Inter99 study cohort (5,965 subjects) and in 332 nondiabetic subjects and 1,063 patients with type 2 diabetes. In the Inter99 cohort, the GCK –30A allele was associated with increased fasting (P < 0.001) and post–oral glucose tolerance test (OGTT) plasma glucose levels (P < 0.001), and in the same cohort, the GCK –30A allele was more frequent among 1,325 subjects with the metabolic syndrome than among 1,679 subjects without any components of the metabolic syndrome (P = 0.002). Moreover, the GCK –30A allele frequency was higher among 2,587 subjects with impaired glucose regulation (IGR) than among 4,773 glucose-tolerant subjects (17.3% [95% CI 16.2–18.3] vs. 15.0% [14.3–15.7], P < 0.001, odds ratio GG vs. GA 1.21 [1.08–1.36], GG vs. AA 1.62 [1.17–2.24]). In conclusion, the GCK –30G>A polymorphism associates with elevated fasting and post-OGTT glycemia in the middle-aged general population of whites, as well as with IGR and other features of the WHO-defined metabolic syndrome.

Address correspondence and reprint requests to Christian Schack Rose, MSc, Steno Diabetes Center, Niels Steensens Vej 8, NSP1.10, DK-2820 Gentofte, Denmark. E-mail: csro{at}steno.dk

Abbreviations: CAD, coronary artery disease; GCK, glucokinase; IFG, impaired fasting glycemia; IGR, impaired glucose regulation; IGT, impaired glucose tolerance; MAF, minor allele frequency; NGT, normal glucose tolerance; OGTT, oral glucose tolerance test; WHO, World Health Organization


Add to CiteULike CiteULike   Add to Del.icio.us Del.icio.us   Add to Digg Digg   Add to Reddit Reddit   Add to Technorati Technorati    What's this?




HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Diabetes Diabetes Care Clinical Diabetes Diabetes Spectrum
Copyright © 2005 by the American Diabetes Association.