C-Reactive Protein, Insulin Resistance, and Metabolic Syndrome in a Population With a High Burden of Subclinical Infection

Insights from the Genetics of Coronary Artery Disease in Alaska Natives (GOCADAN) study

  1. Barbara V. Howard, PHD1,
  2. Lyle Best, MD2,
  3. Anthony Comuzzie, PHD3,
  4. Sven O. E. Ebbesson, PHD4,
  5. Stephen E. Epstein, MD1,
  6. Richard R. Fabsitz, PHD5,
  7. Wm. James Howard, MD6,
  8. Angela Silverman, CNP1,
  9. Hong Wang, MS, MD1,
  10. Jianhui Zhu, PHD1 and
  11. Jason Umans, MD, PHD1
  1. 1MedStar Research Institute, Hyattsville, Maryland
  2. 2Missouri Breaks Industries Research Inc, Timber Lake, South Dakota
  3. 3Southwest Foundation for Biomedical Research, San Antonio, Texas
  4. 4Norton Sound Health Corporation, Nome, Alaska
  5. 5National Heart, Lung, and Blood Institute, Bethesda, Maryland
  6. 6Washington Hospital Center, Washington, DC
  1. Corresponding author: Barbara V. Howard, barbara.v.howard{at}medstar.net

Abstract

OBJECTIVE—To explore relationships between C-reactive protein (CRP), subclinical infection, insulin resistance, and metabolic syndrome.

RESEARCH DESIGN AND METHODS—Data from 1,174 Eskimos, aged ≥18 years, from the Genetics of Coronary Artery Disease in Alaska Natives (GOCADAN) study were analyzed; 40 participants with diabetes were eliminated. Baseline assessment included interviews, physical exam, and blood and urine sampling. Metabolic syndrome was assessed using Adult Treatment Panel III criteria. CRP and antibodies to common pathogens were measured.

RESULTS—Although CRP was related in univariate analyses to insulin resistance and metabolic syndrome, relations were attenuated or eliminated after adjustment for relevant covariates. CRP was not higher among those with impaired fasting glucose (IFG), and pathogen burden was not related to insulin resistance, metabolic syndrome, or IFG.

CONCLUSIONS—Pathogen burden and inflammation do not seem to be related to insulin resistance, metabolic syndrome, or IFG in this population. The inflammatory process may reflect insulin resistance or its correlates but most likely is not causative.

Footnotes

  • Published ahead of print at http://care.diabetesjournals.org on 16 September 2008.

    Readers may use this article as long as the work is properly cited, the use is educational and not for profit, and the work is not altered. See http://creativecommons.org/licenses/by-nc-nd/3.0/ for details.

    The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked “advertisement” in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

    • Accepted September 5, 2008.
    • Received April 29, 2008.
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  1. Published online before print September 16, 2008, doi: 10.2337/dc08-0815 Diabetes Care December 2008 vol. 31 no. 12 2312-2314
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