Special Feature

User Panel

My Panel

My Panel

Bookmark Science Articles

Recent News
Bookmark / Share This Science Site

Association of oxidative stress, insulin resistance, and diabetes risk phenotypes: the Framingham Offspring Study.

Association of oxidative stress, insulin resistance, and diabetes risk phenotypes: the Framingham Offspring Study. Research Abstract Details 

Research Abstract Table of Contents

Jump to the:

  • Abstract Text of This Paper
  • Journal Published
  • MeSH Keywords of This Abstract
  • Chemicals and Substances Used in this Paper
  • Grants and Granting Agency of this Research
  • Database Accession Numbers Used in this Paper
  • Related Papers
  • Related Research Tags
  • Rate this Research Paper
  • Association of oxidative stress, insulin resistance, and diabetes risk phenotypes: the Framingham Offspring Study. Abstract Text:

    james b meigsJames B Meigs,martin g larsonMartin G Larson,caroline s foxCaroline S Fox,john f keaneyJohn F Keaney,ramachandran s vasanRamachandran S Vasan,emelia j benjaminEmelia J Benjamin,

    OBJECTIVE: Systemic oxidative stress causes insulin resistance in rodents. We tested the hypothesis that oxidative stress and insulin resistance are associated in humans. RESEARCH DESIGN AND METHODS: We used cross-sectional data from 2,002 nondiabetic subjects of the community-based Framingham Offspring Study. We measured insulin resistance with the homeostasis model and defined categorical insulin resistance as homeostasis model assessment of insulin resistance (HOMA-IR) > 75th percentile. We measured oxidative stress using the ratio of urine 8-epi-prostaglandin F2alpha (8-epi-PGF2alpha) to creatinine and used age- and sex-adjusted regression models to test the association of oxidative stress with insulin resistance in individuals without diabetes and among subgroups at elevated risk of diabetes. RESULTS: Across 8-epi-PGF2alpha/creatinine tertiles, the prevalence of insulin resistance increased (18.0, 27.5, and 29.4% for the first, second, and third tertiles, respectively; P < 0.0001), as did mean levels of HOMA-IR (3.28, 3.83, and 4.06 units; P < 0.0001). The insulin resistance-oxidative stress association was attenuated by additional adjustment for BMI (P = 0.06 across tertiles for insulin resistance prevalence; P = 0.004 for mean HOMA-IR). Twenty-six percent of participants were obese (BMI > or = 30 kg/m2), 39% had metabolic syndrome (according to the Adult Treatment Panel III definition), and 37% had impaired fasting glucose (IFG) (fasting glucose 5.6-6.9 mmol/l). Among 528 obese participants, respectively, insulin resistance prevalence was 41.3, 60.6, and 54.2% across 8-epi-PGF2alpha/creatinine tertiles (P = 0.005); among 781 subjects with metabolic syndrome, insulin resistance prevalence was 41.3, 56.7, and 51.7% (P = 0.0025); and among 749 subjects with IFG, insulin resistance prevalence was 39.6, 47.2, and 51.6% (P = 0.04). CONCLUSIONS: Systemic oxidative stress is associated with insulin resistance in individuals at average or elevated risk of diabetes even after accounting for BMI.

    Association of oxidative stress, insulin resistance, and diabetes risk phenotypes: the Framingham Offspring Study. Publishing Authors By Initials

    jb meigsJB Meigs,mg larsonMG Larson,cs foxCS Fox,jf keaneyJF Keaney,rs vasanRS Vasan,ej benjaminEJ Benjamin,

    For similar investigative techniques: epidemiologic methods: data collection: vital statistics: morbidity: prevalence research abstracts see: investigative techniques: epidemiologic methods: data collection: vital statistics: morbidity: prevalence research

    PUBMED ID PMID:

    MEDLINE DATE:

    Association of oxidative stress, insulin resistance, and diabetes risk phenotypes: the Framingham Offspring Study. Journal Published:

    PUBLICATION TYPE: Research Support, Non-U.S. Gov

    Journal: Diabetes care

    VOLUME: 30

    Page Numbers: 2529-35

    Journal Abbreviation: Diabetes Care

    ISSN: 1935-5548

    DAY: 22

    MONTH: 06

    YEAR: 2007

    Association of oxidative stress, insulin resistance, and diabetes risk phenotypes: the Framingham Offspring Study. Information

    Number of References:

    LANGUAGE: eng

    NlmUniqueID: 7805975

    Association of oxidative stress, insulin resistance, and diabetes risk phenotypes: the Framingham Offspring Study. Keywords Mesh Terms:

    KEYWORDS: Prevalence

    MESH TERMS: epidemiology

    Chemical & Substance for Abstract: Association of oxidative stress, insulin resistance, and diabetes risk phenotypes: the Framingham Offspring Study. Information

    Substance Name: Creatinine

    Registry Number: 60-27-5

    Grant and Affiliation Information for Association of oxidative stress, insulin resistance, and diabetes risk phenotypes: the Framingham Offspring Study.

    AFFILIATION: General Medicine Division and Department of Medicine, Massachusetts General Hospital and Harvard Medical School, Boston, Massachusetts 02114, USA. jmeigs@partners.org

    Country: United States

    United States Research PublicationUnited States Research Publication

    AGENCY: United States NHLBI

    GRANT: N01-HC-25195

    ACRONYM: HC

    MEDLINETA: Diabetes Care

    REFSOURCE:

    DATABASENAME:

    ACCESSION NUMBER:

    Number Hits: 0

    Association of oxidative stress, insulin resistance, and diabetes risk phenotypes: the Framingham Offspring Study Related Publications

     

    Molecular Station USER Menu

    Welcome to Molecular Station!

    You have to register before you can post on our forums or use our advanced features. Register Now! Its Free and Fast!

    Already registered? Login now below.

    User Name:

    Password:

    Already registered and Forgot your password? Click below to recover it.

    Recover Lost Password

    Join now - it's fast and free!

    Molecular Station is THE largest network of researchers, scientists and science lovers anywhere!

    Research Terms of Usage and Disclaimer
    Home
    Features

    Protocols

    DNA Forum

    Science Forum

    DNA Forum
    Biology Forum

    Science News


    [CaRP] XML error: Invalid document end at line 2

    For more click here:Science News