Literature DB >> 15336815

C-reactive protein concentrations are related to insulin resistance and metabolic syndrome as defined by the ATP III report.

Won-Young Lee1, Jeong-Sik Park, Sang-Young Noh, Eun-Jung Rhee, Ki-Chul Sung, Bum-Soo Kim, Jin-Ho Kang, Sun-Woo Kim, Man-Ho Lee, Jung-Ro Park.   

Abstract

BACKGROUND: C-reactive protein (CRP), very sensitive acute phase reactant, is an important marker of coronary artery disease. However, the relationship between insulin resistance and CRP has not been thoroughly studied. We observed the association between CRP, insulin resistance and metabolic syndrome as defined by the ATP III report, and thus identified the role of CRP in the relation to insulin resistance.
METHODS: Seven hundred and sixty-seven subjects (436 men, 331 women) who underwent a medical check-up at health promotion center in a University Hospital during March 2002, aged 20-84 years, were included in this study. The components of metabolic syndrome as defined by the ATP III report and high sensitivity CRP levels were analyzed, and Homeostasis model assessment index (HOMA) and quantitative insulin sensitivity check index (QUICKI) were calculated.
RESULTS: The mean concentrations of CRP in subjects according to the presence of 0, 1, 2, 3, 4, or 5 components of metabolic syndrome as defined by ATP III were 0.64, 0.95, 1.14, 1.19, 2.40, and 2.53 mg/l, respectively. The mean concentrations of CRP were significantly higher in subjects with a high insulin resistance (higher HOMA index and lower QUICKI) than in those with a low insulin resistance. Significant positive correlations were identified between CRP and BMI, waist circumference, triglyceride, blood pressure, glucose and HOMA index. A significant negative correlation was found between CRP and HDL cholesterol or QUICKI.
CONCLUSION: These results suggest that metabolic syndrome and insulin resistance are associated with systemic inflammatory response, which plays an important pathogenic role in atherosclerosis. Copyright 2004 Elsevier Ireland Ltd.

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Year:  2004        PMID: 15336815     DOI: 10.1016/j.ijcard.2003.08.016

Source DB:  PubMed          Journal:  Int J Cardiol        ISSN: 0167-5273            Impact factor:   4.164


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