Urinary F2-isoprostanes are not associated with increased risk of type 2 diabetes.

Published

Journal Article

OBJECTIVE: Free radicals have been implicated in the etiology of type 2 diabetes. Cross-sectional studies have demonstrated associations between oxidative damage and type 2 diabetes. However, no prospective data on this association are available. RESEARCH METHODS AND PROCEDURES: A case control study was conducted within the prospective cohort of the Insulin Resistance Atherosclerosis Study: 26 cases who developed type 2 diabetes in the follow-up period and 26 controls who remained free of type 2 diabetes were randomly selected. Oxidative status was assessed by measuring 2,3-dinor-5,6-dihydro-15-F2t-isoprostane (F2-IsoPM) in baseline urine samples using gas chromatography/mass spectroscopy. Type 2 diabetes was defined by serial oral glucose tolerance tests and World Health Organization criteria. RESULTS: Urinary F2-IsoPM varied between 0.18 and 2.60 ng/mg creatinine; 25th/50th/75th percentiles were 0.42, 0.60, and 0.89, respectively. A trend toward higher levels were observed in women and in persons with impaired glucose tolerance at baseline (p = 0.1). F2-IsoPM increased with BMI (r = 0.36, p = 0.01). After adjustment for age, gender, baseline impaired glucose tolerance status, and BMI, F2-IsoPM levels were inversely associated with development of type 2 diabetes: odds ratio = 0.32 (95% confidence interval, 0.12 to 0.81) for the difference between the 75th and 25th percentiles. DISCUSSION: These results suggest that oxidative damage is not a cause of type 2 diabetes. Positive cross-sectional associations of F2-IsoPM with the risk factors for diabetes, BMI, and impaired glucose tolerance and inverse associations with development of type 2 diabetes indicate that F2-IsoPM might reflect a compensatory mechanism.

Full Text

Duke Authors

Cited Authors

  • Il'yasova, D; Morrow, JD; Wagenknecht, LE

Published Date

  • September 2005

Published In

Volume / Issue

  • 13 / 9

Start / End Page

  • 1638 - 1644

PubMed ID

  • 16222068

Pubmed Central ID

  • 16222068

International Standard Serial Number (ISSN)

  • 1071-7323

Digital Object Identifier (DOI)

  • 10.1038/oby.2005.201

Language

  • eng

Conference Location

  • United States