C-Reactive Protein, Insulin Resistance, and Metabolic Syndrome in a Population with a High Burden of Subclinical Infection: Insights from the GOCADAN Study

  1. Barbara V. Howard, PhD (Barbara.V.Howard{at}MedStar.net)1,
  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, MD, MS1,
  10. Jianhui Zhu, PhD1 and
  11. Jason Umans, MD, PhD1
  1. 1MedStar Research Institute, Hyattsville, MD
  2. 2Missouri Breaks Industries Research Inc, Timber Lake, SD
  3. 3Southwest Foundation for Biomedical Research, San Antonio, TX
  4. 4Norton Sound Health Corporation, Nome, AK
  5. 5National Heart, Lung, and Blood Institute, Bethesda, MD
  6. 6Washington Hospital Center, Washington, DC

    Abstract

    Objective: To explore relationships among C-reactive protein (CRP), subclinical infection, insulin resistance (IR), and metabolic syndrome (MS).

    Research Design and Methods: Data from 1,174 Eskimos, ≥ age 18, from the Genetics of Coronary Artery Disease in Alaska Natives study were analyzed; 40 participants with diabetes were eliminated. Baseline assessment included interviews, physical exam, and blood and urine sampling. MS was assessed using ATP-III criteria. CRP and antibodies to common pathogens were measured.

    Results: Although CRP was related in univariate analyses to IR and MS, 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 IR, MS, or IFG.

    Conclusions: Pathogen burden and inflammation do not seem related to IR, MS, or IFG in this population. The inflammatory process may reflect IR or its correlates but probably is not causative.

    Footnotes

      • Received April 29, 2008.
      • Accepted September 5, 2008.